Monitoring in Anesthesia and Perioperative Care

Monitoring in Anesthesia and Perioperative Care Monitoring in Anesthesia and Perioperative Care is a practical and comprehensive resource documenting the current art and science of perioperative patient monitoring, addressing the systems-based practice issues that drive the highly regulated health care industry of the early 21st century. Initial chapters cover the history, medicolegal implications, validity of measurement, and education issues relating to monitoring. The core of the book addresses the many monitoring modalities, with the majority of the chapters organized in a systematic fashion to describe technical concepts, parameters monitored, evidence of utility, complications, credentialing and monitoring standards, and practice guidelines. Describing each device, technique, and principle of clinical monitoring in an accessible style, Monitoring in Anesthesia and Perioperative Care is full of valuable advice from the leading experts in the field, making it an essential tool for every anesthesiologist. David L. Reich, M.D. was named Professor and Chair of Anesthesiology at the Mount Sinai School of Medicine in New York in 2004, where he had been Co-Director of Cardiothoracic Anesthesia since 1990. Dr. Reich’s research interests include neurocognitive outcome following thoracic aortic surgery, outcome effects of intraoperative hemodynamics, medical informatics, and hemodynamic monitoring. He has published more than 90 peer-reviewed articles and more than 30 book chapters, and he is an associate editor of the text Cardiac Anesthesia and editor-in-chief of Seminars in Cardiothoracic and Vascular Anesthesia. He is a member of the International Organization for Terminology in Anesthesia (IOTA) of the Anesthesia Patient Safety Foundation and works with that group, the International Health Terminology Standards Development Organisation (IHTDSO), and High Level Seven International (HL7) to create international standards for anesthesia terminology for electronic patient records. Ronald A. Kahn, M.D. is Professor of Anesthesiology and Surgery at the Mount Sinai School of Medicine. Alexander J. C. Mittnacht, M.D. is Associate Professor of Anesthesiology at the Mount Sinai School of Medicine and Director of Pediatric Cardiac Anesthesia at the Mount Sinai Medical Center. Andrew B. Leibowitz, M.D. is Professor of Anesthesiology and Surgery at the Mount Sinai School of Medicine and Executive Vice Chairman of the Department of Anesthesiology at the Mount Sinai Medical Center. Marc E. Stone, M.D. is Associate Professor of Anesthesiology at the Mount Sinai School of Medicine and Program Director of the Fellowship in Adult Cardiothoracic Anesthesiology at the Mount Sinai Medical Center. James B. Eisenkraft, M.D. is Professor of Anesthesiology at the Mount Sinai School of Medicine and Attending Anesthesiologist at the Mount Sinai Medical Center.

Monitoring in Anesthesia and Perioperative Care Editor David L. Reich Mount Sinai School of Medicine

Coeditors Ronald A. Kahn Mount Sinai School of Medicine

Alexander J. C. Mittnacht Mount Sinai School of Medicine

Andrew B. Leibowitz Mount Sinai School of Medicine

Marc E. Stone Mount Sinai School of Medicine

James B. Eisenkraft Mount Sinai School of Medicine

CAMBRID GE UNIVERSIT Y PRESS Cambridge, New York, Melbourne, Madrid, Cape Town, Singapore, S˜ao Paulo, Delhi, Tokyo, Mexico City Cambridge University Press 32 Avenue of the Americas, New York, NY 10013-2473, USA www.cambridge.org Information on this title: www.cambridge.org/9780521755986  C Cambridge University Press 2011

This publication is in copyright. Subject to statutory exception and to the provisions of relevant collective licensing agreements, no reproduction of any part may take place without the written permission of Cambridge University Press. First published 2011 Printed in the United States of America A catalog record for this publication is available from the British Library. Library of Congress Cataloging in Publication data Monitoring in anesthesia and perioperative care / [edited by] David L. Reich, Ronald A. Kahn, Alexander J. C. Mittnacht, Andrew B. Leibowitz, Marc E. Stone, James B. Eisenkraft. p.; cm. Includes bibliographical references and index. ISBN 978-0-521-75598-6 (hardback) 1. Anesthesia. 2. Patient monitoring. I. Reich, David L. (David Louis), 1960– , editor. II. Kahn, Ronald A., editor. III. Mittnacht, Alexander J. C., editor. IV. Leibowitz, Andrew B., editor. V. Stone, Marc E., editor. VI. Eisenkraft, James B., editor. [DNLM: 1. Monitoring, Intraoperative – methods. 2. Anesthesia – methods. 3. Perioperative Care – methods. WO 181] RD82.M68 2011 617.9 6–dc22 2010045695 ISBN 978-0-521-75598-6 Hardback Cambridge University Press has no responsibility for the persistence or accuracy of URLs for external or third-party Internet Web sites referred to in this publication and does not guarantee that any content on such Web sites is, or will remain, accurate or appropriate. Every effort has been made in preparing this book to provide accurate and up-to-date information that is in accord with accepted standards and practice at the time of publication. Although case histories are drawn from actual cases, every effort has been made to disguise the identities of the individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that the information contained herein is totally free from error, not least because clinical standards are constantly changing through research and regulation. The authors, editors, and publishers therefore disclaim all liability for direct or consequential damages resulting from the use of material contained in this book. Readers are strongly advised to pay careful attention to information provided by the manufacturer of any drugs or equipment that they plan to use.

Contents Contributors vii Foreword by Carol L. Lake Preface xii

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1

The history of anesthesia and perioperative monitoring 1 David L. Reich

15 Monitoring pressure, volume, and flow in the anesthesia breathing system 171 James B. Eisenkraft

2

Medicolegal implications of monitoring Jeffrey M. Feldman

16 Pulse oximetry 185 Tuula S. O. Kurki and James B. Eisenkraft

3

Validity, accuracy, and repeatability of monitoring variables 16 Daniel M. Thys and Jung Kim

17 Neurologic intraoperative electrophysiologic monitoring 199 Michael L. McGarvey and Albert T. Cheung

4

Teaching monitoring skills 27 Samuel DeMaria, Jr., Adam I. Levine, and Yasuharu Okuda

18 Level of consciousness monitoring Marc J. Bloom

5

Electrocardiography 36 Alexander J. C. Mittnacht and Martin London

6

Arterial pressure monitoring 45 Alexander J. C. Mittnacht and Tuula S. O. Kurki

7

Central venous and pulmonary artery catheterization 57 Deborah Dubensky and Alexander J. C. Mittnacht

8

Cardiac output and intravascular volume Mukul Kapoor and Marc E. Stone

9

Gastric tonometry 95 Elliott Bennett-Guerrero

9

19 Transcranial Doppler Dean B. Andropoulos

21 Near-infrared spectroscopy Dean B. Andropoulos

23 Critical care testing in the operating room: electrolytes, glucose, acid–base, blood gases Lakshmi V. Ramanathan, Judit Tolnai, and Michael S. Lewis

150

281

24 Laboratory-based tests of blood clotting 291 Nathaen Weitzel, Tamas Seres, and Glenn P. Gravlee

11 Transesophageal echocardiography 105 Ronald A. Kahn and Gregory W. Fischer

14 Respiratory gas monitoring James B. Eisenkraft

249

22 Perioperative monitoring of neuromuscular function 261 Aaron F. Kopman

10 Oxygen delivery, oxygen transport, and tissue oxygen tension: critical monitoring in the ICU 98 Jayashree Raikhelkar and Peter J. Papadakos

13 Ultrasound guidance for regional anesthesia procedures 145 Christina L. Jeng and Meg A. Rosenblatt

226

20 Multimodality monitoring in critically ill neurologic patients 237 Jennifer A. Frontera

79

12 Ultrasound guidance of vascular catheterization Andrew B. Leibowitz and Jonathan Elmer

218

136

25 Coagulation and hematologic point-of-care testing 308 Liza J. Enriquez and Linda Shore-Lesserson 26 Cardiac biomarkers for perioperative management 319 Anoushka Afonso and Eric Adler 27 Endocrine testing in the operating room 327 Lakshmi V. Ramanathan and Michael S. Lewis

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Contents

28 Temperature monitoring 331 David Wax and Justin Lipper

34 Intensive care unit risk scoring 369 Adel Bassily-Marcus and Roopa Kohli-Seth

29 Fetal heart rate monitoring Howard H. Bernstein

35 Computers and monitoring: information management systems, alarms, and drug delivery 383 David Wax and Matthew Levin

337

30 Pain scales 348 Jonathan Epstein, Diana Mungall, and Yaakov Beilin 31 Neurologic clinical scales Jennifer A. Frontera

353

32 Postanesthesia care unit assessment scales David Bronheim and Richard S. Gist 33 Delirium monitoring: scales and assessments Brigid Flynn and Corey Scurlock

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357 360

Appendix: Monitoring recommendations for common types of surgical procedures 397 Index 405 Color plates follow page 260.

Contributors

Eric Adler, M.D. Assistant Professor Department of Cardiology Mount Sinai School of Medicine New York, NY Anoushka Afonso, M.D. Anesthesia Resident Department of Anesthesiology Mount Sinai School of Medicine New York, NY Dean B. Andropoulos, M.D., M.H.C.M. Chief of Anesthesiology Texas Children’s Hospital Professor, Anesthesiology and Pediatrics Baylor College of Medicine Houston, TX Adel Bassily-Marcus, M.D. Assistant Professor Department of Surgery Division of Critical Care Medicine Mount Sinai School of Medicine New York, NY Yaakov Beilin, M.D. Professor Department of Anesthesiology Department of Obstetrics, Gynecology, and Reproductive Science Mount Sinai School of Medicine New York, NY

Marc J. Bloom, M.D., Ph.D. Associate Professor of Anesthesiology New York University School of Medicine New York, NY David Bronheim, M.D. Associate Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Albert T. Cheung, M.D. Professor Department of Anesthesiology and Critical Care University of Pennsylvania School of Medicine Philadelphia, PA Samuel DeMaria, Jr., M.D. Instructor in Anesthesiology Department of Anesthesiology Mount Sinai School of Medicine New York, NY Deborah Dubensky, M.D. Department of Anesthesiology University of Rochester Medical Center Rochester, NY James B. Eisenkraft, M.D. Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Elliott Bennett-Guerrero, M.D. Professor and Director of Perioperative Clinical Research Duke Clinical Research Institute Duke University Medical Center Durham, NC

Jonathan Elmer, M.D. Clinical Fellow Department of Emergency Medicine Brigham and Women’s Hospital Boston, MA

Howard H. Bernstein, M.D. Associate Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Liza J. Enriquez, M.D. Fellow Department of Anesthesiology Montefiore Medical Center Bronx, NY

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Contributors

Jonathan Epstein, M.D., M.A. Attending Anesthesiologist St. Luke’s–Roosevelt Hospital Center New York, NY Jeffrey M. Feldman, M.D., M.S.E. Associate Professor of Clinical Anesthesiology Department of Anesthesiology and Critical Care Medicine University of Pennsylvania School of Medicine Division Chief, General Anesthesia Children’s Hospital of Philadelphia Philadelphia, PA

Mukul Kapoor, M.D. Senior Adviser Anaethesiology and Cardiothoracic Anaesthesiology Command Hospital Lucknkow, India Jung Kim, M.D. Department of Anesthesiology St. Luke’s–Roosevelt Hospital Center New York, NY

Gregory W. Fischer, M.D. Associate Professor of Anesthesiology and Cardiothoracic Surgery Director of Adult Cardiothoracic Anesthesia Mount Sinai School of Medicine New York, NY

Roopa Kohli-Seth, M.D. Assistant Professor Department of Surgery Division of Critical Care Medicine Mount Sinai School of Medicine New York, NY

Brigid Flynn, M.D. Assistant Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Aaron F. Kopman, M.D. Professor of Clinical Anesthesiology Weill Cornell Medical College New York, NY

Jennifer A. Frontera, M.D. Assistant Professor Departments of Neurology and Neurosurgery Mount Sinai School of Medicine New York, NY Richard S. Gist, M.D. Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Glenn P. Gravlee, M.D. Professor Department of Anesthesiology University of Colorado Denver Aurora, CO Christina L. Jeng, M.D. Assistant Professor of Anesthesiology and Orthopaedics Department of Anesthesiology Mount Sinai School of Medicine New York, NY Ronald A. Kahn, M.D. Professor of Anesthesiology Department of Anesthesiology Mount Sinai School of Medicine New York, NY

viii

Jenny Kam, M.D. Chief Resident Department of Anesthesiology

Tuula S. O. Kurki, M.D., Ph.D. Head of the Preoperative Clinic Department of Anesthesia and Intensive Care Helsinki University Central Hospital Helsinki, Finland Andrew B. Leibowitz, M.D. Professor of Anesthesiology and Surgery Department of Anesthesiology Mount Sinai School of Medicine New York, NY Matthew Levin, M.D. Mount Sinai School of Medicine New York, NY Adam I. Levine, M.D. Associate Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Michael S. Lewis, M.D. Director of Transfusion Medicine and Histology Assistant Professor of Pathology University of Southern California, Keck School of Medicine Attending Pathologist West Los Angeles VA Hospital Mount Sinai School of Medicine Los Angeles, CA

Contributors

Justin Lipper, M.D. Mount Sinai School of Medicine New York, NY

Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Martin London, M.D. Professor of Clinical Anesthesia University of California, San Francisco San Francisco, CA

Meg A. Rosenblatt, M.D. Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Michael L. McGarvey, M.D. Assistant Professor Department of Neurology University of Pennsylvania Philadelphia, PA Alexander J. C. Mittnacht, M.D. Associate Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Timothy Mooney, MD Fellow Duke University Medical Center Durham, NC Diana Mungall, B.S. Department of Anesthesiology Mount Sinai School of Medicine New York, NY Yasuharu Okuda, M.D. Associate Clinical Professor Department of Emergency Medicine Mount Sinai School of Medicine New York, NY Peter J. Papadakos, M.D., F.C.C.M. Professor of Anesthesiology, Surgery, and Neurosurgery Director, Division of Critical Care Medicine University of Rochester Rochester, NY Jayashree Raikhelkar, M.D. Assistant Professor Departments of Anesthesiology and Cardiothoracic Surgery Mount Sinai School of Medicine New York, NY Lakshmi V. Ramanathan, Ph.D. Assistant Professor Department of Pathology Mount Sinai School of Medicine Director, Chemistry, Endocrinology, Stat Lab, and Point of Care Testing Mount Sinai Medical Center New York, NY David L. Reich, M.D. Professor and Chair of Anesthesiology

Corey Scurlock Assistant Professor Departments of Anesthesiology and Cardiothoracic Surgery Mount Sinai School of Medicine New York, NY Tamas Seres, Ph.D. Associate Professor Department of Anesthesiology University of Colorado Denver Aurora, CO Linda Shore-Lesserson, M.D. Professor of Anesthesiology Montefiore Medical Center Bronx, NY Marc E. Stone, M.D. Associate Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Daniel M. Thys, M.D. Chairman Emeritus Department of Anesthesiology St. Luke’s–Roosevelt Hospital Center New York, NY Judit Tolnai, B.S. Department of Pathology Mount Sinai School of Medicine New York, NY David Wax, M.D. Assistant Professor Department of Anesthesiology Mount Sinai School of Medicine New York, NY Nathaen Weitzel, M.D. Assistant Professor Department of Anesthesiology University of Colorado Denver Aurora, CO

ix

Foreword Carol L. Lake

Training and practicing the specialty of anesthesiology, and specifically cardiac anesthesia, during the last three decades of the 20th century provides a unique perspective from which to address the state of clinical monitoring for health care. The advent and growth of sophisticated physiologic monitoring clearly advanced the anesthesiology subspecialty of cardiac anesthesia, and vice versa. Likewise, it seems especially prudent that Dr. David L. Reich, a cardiac anesthesiologist, and many of the chapter authors, represent the subspecialty of cardiac anesthesia. From using a manual blood pressure cuff, precordial stethoscope, and a finger on the pulse to the current American Society of Anesthesiologists standards of monitoring the patient’s oxygenation, ventilation, circulation, and temperature continually (usually with pulse oximetry, electrocardiogram, end-tidal carbon dioxide, temperature, inspired/expired anesthetic gases, and automated blood pressure cuff during general anesthesia) was the great leap forward in perioperative monitoring in the 20th century. Similarly, the plethora of devices developed during the past century to allow monitoring of depth of anesthesia, respiratory compliance, ventricular contractility, coagulation, tissue oxygenation, and blood flow, rather than only basic cardiovascular parameters such as heart rate and blood pressure, is truly amazing progress. The past and present of physiologic monitoring are represented in the history chapter and the chapters on equipment, procedures, techniques, and technologies, respectively, in this book. Unfortunately, at the present time, many of the critical incidents during anesthesia still result from inadequate or incomplete monitoring of the patient, the anesthesia machine, or the patient–machine interface. What is the future for monitoring in health care in general and anesthesiology, critical care, and pain management in particular? With the miraculous advances in clinical monitoring have come associated challenges that are addressed in this book. How can information overload from monitors be minimized? How are trainees educated and trained in multiple monitoring techniques? How can practitioners beyond training maintain their skills with infrequently used, complex monitors? How will future anesthesiologists and intensivists know whether a new device or monitoring technique is useful and reliable? Has a cost–benefit analysis of a specific monitor demonstrated effectiveness? Similar demanding questions need to be answered. Finally, is the ongoing research to develop new

x

devices or techniques to monitor parameters currently judged difficult to assess, such as intraoperative, global cerebral or renal function, being adequately supported? Dr. Reich and his many distinguished contributing authors provide a comprehensive practical review of these questions while preparing the reader to confront these future monitoring challenges. Information overload occurs when there are many parameters to observe, necessitating the provision of alarm systems, set to indicate when a particular parameter or device is outside set limits. However, these same alarms do not always indicate true life-threatening emergencies. Attending to false alarms adds to the workload and encourages ignoring them, obviously to the detriment of the patient if the alarm is not false. Ways to prioritize and display alarms, and to prevent unnecessary alarms, will continue to be the subject of research until user-friendly, ergonomic, common anesthesia workstations exist. Reliance on alarms may also encourage inattention by the person providing anesthesia or critical care. Although a recent single-institution study demonstrated that intraoperative reading and nonpatient-related conversation did not adversely affect recognition of a randomly illuminated alarm light (Slagle JM, Weinger MB. Effects of intraoperative reading on vigilance and workload during anesthesia care in an academic medical center. Anesthesiology 2009;110:275–283), recognizing an impending disaster before the alarm sounds may save precious seconds, and those seconds count if you or your loved one is the anesthetized or critically ill patient. The training, retraining, and ongoing evaluation of competence of the anesthesia team to use complex and sophisticated monitoring devices remains an educational conundrum. Although textbooks and lectures continue to be the mainstay of health care educational material, interactive computer programs; standardized patients; part-task trainers; human patient simulators mimicking neonates, children, and adults; and realistic simulation laboratories configured to be operating rooms, intensive care units, emergency departments, or patient rooms appear likely to become the major training and examination venues in the 21st century. A simulation laboratory is an ideal environment to learn to use monitoring devices and techniques and is particularly applicable to demonstration of competence with monitoring techniques. Are there hazards to the extensive use of monitoring? Possibly. Could the increased technology of monitoring occur at

Foreword

the expense of clinical acumen? We have already seen that overreliance on monitors leads to both amusing and deleterious situations, such as the pronouncement of ventricular fibrillation by a new anesthesiology resident when an electrocardiograph lead falls off the patient or the inability to assess anesthetized patient well-being when electrical power is interrupted in a developing country or following a disaster. Could sophisticated 21st-century perioperative monitoring expose the specialty of anesthesiology to eventual substitution by robots with artificial intelligence? Probably not, because the monitors still lack the completeness, continuousness, and adaptability to human natural variation in perioperative situations.

Despite all the extensive and sophisticated devices and techniques described in this book, there is nothing at present that can replace the vigilance of a professional anesthesia or intensive care team providing the human-to-human interaction essential to patient safety and well-being in operating rooms, intensive care units, or the myriad venues in which patients receive general anesthesia or its equivalents. As Dr. Reich’s book aptly illustrates, 21st-century monitoring for anesthesiology, pain management, and critical care must focus on striking the optimal balance among such factors as patient safety, cost, clinical outcomes, innovation, and complexity. However, the patient, not the monitor, must always come first!

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Preface

Monitoring in Anesthesia and Perioperative Care follows the tradition of previous texts that document the current art and science of perioperative patient monitoring. Additionally, the text addresses the systems-based practice issues that drive the highly regulated health care industry of the early 21st century. The initial chapters cover the concepts of history, medicolegal implications, validity of measurement, and education. The core of the book addresses the many monitoring modalities. To the extent possible, each chapter is organized in a systematic fashion to describe: 1. Technical concepts: How does it work? 2. Parameters monitored: What information do you get from it? 3. Evidence of utility: Is there evidence that it makes a difference in outcome? 4. Complications: What harm can it cause? 5. Credentialing and monitoring standards: What is the educational or credentialing process, if any? 6. Practice guidelines: When should/must I use it? Ultrasonic guidance of invasive catheterization and regional anesthesia are included as monitoring concepts. The next group of chapters addresses scales and assessments that are increasingly evidence-based documentation standards. Finally, electronic health records, alarm systems, and automated medication delivery systems complete the body of the text. A table in the appendix is intended to help residents and other anesthesia care providers know the typical monitoring modalities that are chosen for major categories of operations. The target audience for this text is medical students, anesthesia residents, Fellows, nurse anesthetists, anesthesia assistants, and anesthesia and critical care practitioners who are acquiring or updating their knowledge of patient monitoring during anesthesia and the perioperative period. There is significant overlap with critical care monitoring, and the intensive care physician will find nearly all concepts of critical care monitoring to be covered.

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Patient monitoring in anesthesia and perioperative care has changed drastically since the specialty of anesthesiology emerged in the 19th century. The pace of that change has accelerated in recent decades as one sees in the preceding texts on the subject, which are snapshots of the monitoring practices of their eras. The earliest of those texts that I located illustrated an important juncture in the art and science of patient monitoring. In these two quotes from the preface of Dornette and Brechner’s Instrumentation in Anesthesiology (Philadelphia: Lea & Febiger, 1959), we see the point in anesthesia history at which the emphasis shifted from direct patient observation to reliance on mechanical instrumentation: [The anesthesiologist] feels the pulse and rebreathing bag to determine rate, rhythm and volume of the pulse waves and respiratory efforts. He sees the eye signs and thoracic excursions to assess depth of anesthesia. He hears the sound generated by compression of the brachial artery during auscultation of the blood pressure. He smells the anesthetic atmosphere to determine the approximate concentration of ether or cyclopropane. He tastes the fluid dripping from the epidural needle to differentiate bitter procaine from tasteless cerebrospinal fluid. [Instrumentation] increases the perceptibility of our senses, and also allows the study of physiologic signals not capable of being detected by these senses.

The monitoring texts in more recent years, including those edited by Lake, Saidman and Smith, Blitt and Hines, Gravenstein and colleagues, and Dorsch and Dorsch, have chronicled these continuing changes in both instrumentation and standards. Their erudition and eloquence set a high standard. The current publication is intended to continue the tradition of anesthesiologists as the leaders in patient monitoring education and standards creation. David L. Reich, M.D. Professor and Chair Department of Anesthesiology Mount Sinai School of Medicine New York, NY

Chapter

1

The history of anesthesia and perioperative monitoring David L. Reich

Introduction The discoveries that facilitated patient monitoring in the perioperative period occurred long before the introduction of clinical anesthesia. Respiratory patterns had been described since antiquity. The rise of scientific methods in Renaissance Europe led to the initial experiments in hemodynamics – specifically, animal experiments demonstrating that blood flows under pressure. The earliest source that cited correct observations of arterial and venous flow and pressures was William Harvey’s De Motu Cordis, published in 1628.1 In the following century, Stephen Hales offered the first quantification of arterial blood pressure measured in the horse.2 The first cardiac catheterization was performed by Claude Bernard in 1844.3 Soon after the introduction of clinical general anesthesia by W. T. G. Morton in 1846 and John Snow in 1847, the need to monitor patients was recognized by the leaders of the new specialty. The first documented death under chloroform anesthesia (that of fifteen-year-old Hannah Greener in 1848) led the early practitioners to highlight the importance of monitoring simple vital signs – respiration, pulse, and skin color. Since that time, patient safety concerns have invariably driven the development of monitoring modalities and standards in perioperative monitoring practice. This chapter recounts important milestones of perioperative patient monitoring and the historical events and clinical developments that influenced them.

Early advocacy of monitoring the pulse and respiration As news of the Boston public demonstration reached London late in 1846, John Snow, M.D. personally adopted the technique, publishing his series of eighty anesthetized patients, ranging in age from children to octogenarians, in Inhalation of the Vapour of Ether in Surgical Operations. He mentioned the customary monitoring under anesthesia to include respiration depth and frequency, muscle movements, skin color, and stages of excitation or sedation. Although the pulse was continually palpated, its characteristics were not considered worth studying.4 By 1855, the Edinburgh surgeon James Syme, M.D., lectured on the importance of monitoring respiration

and explained in his surgical lectures that, in his opinion, chloroform was safer than ether anesthesia if it was administered properly. The key, however, to proper administration was monitoring the patient’s respiration.5 Joseph Lister, M.D., the founder of the principles of antisepsis in surgery, was an eminent surgeon in Scotland and the United Kingdom from the 1850s through the 1890s. He protested against palpation of the pulse as “a most serious mistake. As a general rule, the safety of the patient will be most promoted by disregarding it altogether, so that the attention may be devoted exclusively to the breathing.”6 Dr. Lister’s instruction to the senior students who served as his anesthetists was “that they strictly carry out certain simple instructions, among which is that of never touching the pulse, in order that their attention may not be distracted from the respiration.” His airway management strategy included “the drawing out of the tongue” and he believed that the services of special anesthetists were unnecessary if simple routines were followed by his assistants while administering chloroform. Joseph Thomas Clover, M.D., was the leading clinical anesthetist in Victorian England during his professional life, from the beginning of his anesthesia practice in 1846 until his death in 1882. In 1864, the Royal Medico-Chirurgical Society established a committee to investigate chloroform fatalities, and as an expert assistant to that group, Dr. Clover described his innovations in apparatus and animal experimentation with anesthetics. He strongly advised that the pulse be continuously observed during an anesthetic and that irregularities such as a diminution should alert the anesthetist to discontinue the anesthetic. He also advised monitoring the pulse continuously while administering an anesthetic. “If the finger be taken from the pulse to do something else, I would give a little air.”7 James Young Simpson, M.D., also voiced caution during the administration of chloroform when snoring ensued and the pulse became “languid.”8 With continuing deaths associated with chloroform use, a group led by Edward Lawrie formed a commission in Hyderabad, India to investigate causes. In 1888, the first commission report asserted the safety of chloroform anesthesia.9 In 1889, the Second Hyderabad Chloroform Commission concluded that chloroform deaths were related to respiratory depression and not a directly injurious effect on the heart. The commission

1

Monitoring in Anesthesia and Perioperative Care

reported that anesthetists should be guided entirely by respiration, as pupil size and pulse were not significant enough to monitor.10,11

Auscultation of heart tones The earliest clinical account of auscultation in the operating room was reported in 1896 by Robert Kirk, M.D., of the Glasgow Western Infirmary. An ordinary binaural stethoscope lengthened by Indian rubber tubing was first used. Later, 200 patients anesthetized with chloroform were auscultated using a “phonendoscope” with timing of heart rate and rhythm by a watch.12 Dr. Kirk was involved at the time with the Glasgow Committee on Anesthetic Agents and saw the stethoscope as a clinical research tool to assess the effects of chloroform on cardiac physiology. Charles K. Teter, D.D.S., described the benefits of using a stethoscope during anesthesia, especially in poor-risk patients.13 He praised the convenience of the flat Kehler stethoscope, which “will usually stay without being held” on the precordium. When necessary, adhesive tape prevented its being dislodged. Dr. Teter praised the stethoscope because “uninterrupted information will be given to any and all change[s] in the heart beat and respiration.” He expressed his feeling of confidence when “every variation of heart sound is at once discernable, and what might be serious complications can be averted by the premonitory symptoms thus made manifest.”13 The strong advocacy of routine, continuous monitoring of cardiac and respiratory sounds under anesthesia by Harvey Cushing, M.D., gave impetus to the widespread clinical use of intraoperative auscultation14 (see Figure 1.1). An esophageal stethoscope was described in 1893 by Solis-Cohen15 for diagnostic purposes, but it was not adopted as a routine monitoring technique until nearly seventy-five years later.

Figure 1.1. Early stethoscopes used for intraoperative monitoring are displayed. (Courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL)

2

The anesthesia record Once the idea that monitoring patients under anesthesia was clinically useful and early tools were developed to do so, the anesthetic record could not be far behind. B. Raymond Fink, M.D., credits the first anesthetic record to A. E. Codman, M.D., at the Massachusetts General Hospital in 189416 (Figure 1.2). Dr. Codman’s chief, F. B. Harrigan, M.D., recommended recording the patient’s pulse during an anesthetic. This practice was encouraged by Dr. Cushing, who published a classic paper in 1902 reproducing an actual patient’s anesthetic record.17 Dr. Cushing’s initiatives were not accepted easily, and opponents to the newer devices to measure temperature, pulse, blood pressure, and the auscultation of the heart were castigated by an editorial in the British Medical Journal claiming that “by such methods we pauperize our senses and weaken clinical acuity.”18

Indirect measurement of arterial blood pressure In 1901, during a visit to Italy, Harvey Cushing met Scipione Riva-Rocci, who, a few years earlier, had developed a practical sphygmomanometer for measuring blood pressure indirectly.19 Subsequently, Cushing recommended the routine use of this sphygmomanometer to determine blood pressure during anesthesia.20 Because the return-to-flow method was employed by palpation of the radial pulse, only the systolic pressure could be determined. Furthermore, this was inaccurate, as the cuff used was a bicycle inner tube, which gave excessively high values owing to the ratio of the region of compression to arm circumference. At that time, however, normal values for systolic blood pressure were unknown and the instrument provided the first clinical example of following trends of blood pressure change during surgery. In 1905, Korotkoff described the sounds heard when flow occurs distal to the deflating cuff.21 This, together with the use of a wider cuff advocated by von Recklinghausen,22 allowed more accurate determination of blood pressure and is the basis of current auscultatory blood pressure monitoring. Further advances in the indirect measurement of blood pressure largely involved the development of alternative means of “sensing” systolic and diastolic points and automating the process. In 1931, von Recklinghausen23 described a semiautomated device for measuring blood pressure, known as an oscillotonometer. A double-cuff system was used, with the proximal cuff occluding the artery and the distal cuff acting as the sensor to detect the onset of arterial pulsations. The introduction of ultrasound into clinical medicine in the 1940s allowed the application of the Doppler principle to detect blood flow24 and movement of the arterial wall under the distal edge of the sphygmomanometer cuff.25 The Arteriosonde (Roche) used ultrasound at 3 mHz that reflected off the vibrating arterial wall, which the practitioner heard as an electronically conditioned audible signal. The device was accurate and found its greatest application for measurement of blood pressure in infants.26 The

Chapter 1 – The History of Anesthesia and Perioperative Monitoring

Figure 1.2. One of the first known anesthesia records is reproduced. (Courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL)

desire for more automated and rapid acquisition of noninvasive blood pressure led to the development of automated devices has allowed frequent estimation of indirect blood pressure. The first wide commercial success was the Dinamap (Critikon), which essentially was an automated oscillotonometer. The instrument was simple to use and produced accurate results.27

Eye signs of anesthesia depth Although Snow and other early leaders of the specialty described the monitoring of depth of anesthesia, the individual given greatest credit for standardizing the process was Arthur Guedel, M.D. The eye signs of ether anesthesia were the most significant contribution to his schematic approach to identifying signs of anesthesia.28 The eye signs included the activity of motor muscles of the eyeball, pupillary dilation, and, later, the eyelid reflex. The eyelid reflex was tested by gently raising the upper eyelid with the finger. If the reflex was present, the eyelid would attempt to close at once or within a few seconds. The corneal and eyelash reflexes known today were not mentioned.29 The setting for these contributions was the complete lack of trained anesthesia specialists when the United States entered World War I.30 Dr. Guedel experienced a crush of casualties from a major battle, where his staff of three physicians and one dentist ran as many as forty operating room tables at a time. He concluded that additional anesthesia care providers would have to be trained quickly to meet this overwhelming need and

created a school that trained physicians, nurses, and orderlies in open-drop ether.29 He prepared a chart of his version of the signs and stages of ether anesthesia, the most common agent in use at the time because of its wide margin of safety (Figure 1.3). Armed with their charts, the trainees went out to nearby hospitals to work on their own, as Dr. Guedel made weekly motorcycle rounds to check on his trainees at the six hospitals for which he was responsible.30

Direct measurement of arterial blood pressure Poiseuille, in 1828, described the mercury manometer.31 In 1847, Karl Ludwig made use of Poiseuille’s device and applied it to his invention of the kymograph.32 A column of mercury on the kymograph moved, and thus directed a floating needle against a moving drum. This device allowed animal hemodynamic physiology to be recorded continuously for research purposes. The application to humans, however, was limited by problems of vascular access and control of bleeding and infection. Almost one century later, direct recording of arterial blood pressure continued to be difficult, even though problems of sepsis and coagulation were solved. The discovery of plastic “nonthrombogenic” sterile tubing and its medical applications occurred in 1945–46. In 1949, Lyle Peterson and Robert Dripps described the technique of percutaneous placement of a plastic catheter for continuous measurement of arterial blood pressure during anesthesia and surgery.33

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Monitoring in Anesthesia and Perioperative Care

Figure 1.3. One version of Guedel’s chart demonstrating stages of ether anesthesia. (Courtesy of the Wood Library-Museum of Anesthesiology, Park Ridge, IL)

The value of this measurement was widely recognized, but the technique remained unpopular. The recording equipment was impractical and too expensive. The technique of surgical cut-down was used to gain access to peripheral arteries during cardiac surgery in the 1950s. In 1960, the catheter-over-the-needle technique was introduced, and the wide medical application of polytetrafluoroethylene (PTFE; Teflon, Dupont, Inc.) Teflon made possible convenient percutaneous access, leading to easier and smoother percutaneous placement of cannulae for continuous monitoring of arterial blood pressure by surgeons, anesthesiologists, and intensive care specialists. Simultaneous technological advances in pressure transducers, continuous flush systems, and transistor-based display and recording equipment made invasive arterial monitoring commonplace.

The electrocardiogram in the operating room In 1918, Heard and Strauss34 reported two cases of atrioventricular rhythm, one of which occurred immediately following ether anesthesia. They reported that “no other cases of nodal rhythm have been observed by us in a series of 21 cases in which electrocardiographic records have been taken during anesthesia.” No further details were given. Levine35 reported two cases of paroxysmal atrial tachycardia under ether anesthesia, documented by electrocardiography.

4

The first prospective study of the practical use of the electrocardiograph (ECG) for monitoring patients in the operating room was reported in 1922. Lennox, Graves, and Levine36 studied fifty operations performed on forty-nine patients at the Peter Bent Brigham Hospital in Boston. The monitoring method was onerous. The electrocardiographer was summoned by a buzzer in the operating room at the beginning and end of the operation and during critical moments in the operation. ECG tracings were produced by a string galvanometer, at average intervals of 2.5 minutes. For a permanent record, photographic paper had to be exposed to light. The heart rate calculated from the ECG tracings was much higher than the count of the anesthetist. The most marked discrepancies usually occurred during induction of anesthesia, when the pulse rate was taken by a nurse from the ward. Abnormalities of conduction (displacement of pacemaker) were found in 15 (30%) of the cases and 11 cases developed premature beats, seven of them ventricular in origin. None of these premature beats was noted by the anesthetist. Analysis of the patients’ characteristics, type of surgery, and type of anesthesia failed to demonstrate predisposing factors apart from alterations in vagal tone. The value of the electrocardiogram during surgery was demonstrated by further similar studies.37–39 The intermittent nature of the recording and the inevitable delay in developing ECG tracings on photographic paper, however, limited the usefulness of these observations for diagnosis and therapy.

Chapter 1 – The History of Anesthesia and Perioperative Monitoring

Direct-writing ECG recorders eliminated the delay associated with processing films but were impractical for obtaining continuous records.40 In 1952, Himmelstein and Scheiner described a cardiotachoscope, which permitted continuous display of the ECG on a cathode ray screen.41 The heart rate, obtained by measuring the time interval between successive beats, appeared as a moving line on the calibrated screen of a cathode ray tube. A direct writing cardiograph could be attached to the instrument to obtain permanent records. With the advent of continuous ECG monitoring devices, the routine use of the ECG to detect abnormalities of rhythm and rate became practical, albeit too expensive for routine use. Several reviews and studies42,43 documented the type and incidence of dysrhythmias that could occur during anesthesia. Lead II was usually monitored because the axis paralleled the normal P wave vector, facilitating easy recognition of dysrhythmias. The application of the ECG to detect myocardial ischemia during anesthesia was first proposed by Kaplan and King.44 In patients undergoing stress tests, Blackburn45 had previously found that the majority of ischemic episodes could be detected by precordial lead V5 of a 12-lead electrocardiogram. Kaplan46 demonstrated successful use of a modified CM5 lead in anesthetized patients. This lead was practical with three-lead ECG systems, then in common clinical use in the operating room.

Central venous and pulmonary artery catheterization Werner Forssmann is credited with being the first person to pass a catheter into the heart of a living person47 , using himself as the subject. He passed a ureteral catheter through one of his left antecubital veins, guiding it by fluoroscopy into his right atrium, and then confirming the position by chest roentgenogram. In 1930, Klein reported eleven catheterizations of the right side of the heart, including catheterization of the right ventricle and measurement of cardiac output in humans, using Fick’s principle.48 In the 1940s, catheterization of the right side of the heart began to be used to investigate problems of cardiovascular physiology by Cournand,49 who later received the Nobel prize (together with Forssmann) for his pioneering efforts. In 1947, Dexter50 and Werko51 reported on oxygen saturation in the pulmonary artery and demonstrated, for the first time, the value of the pulmonary artery wedge pressure in estimating left atrial pressure. In 1970, a balloon-tipped flowguided catheter technique was introduced by Swan and Ganz, making possible the use of the catheter outside the catheterization laboratory in intensive care units and operating rooms.52

Monitoring of oxygenation, blood gases, and acid–base status As related by John W. Severinghaus, respiratory physiology became important when World War II pilots trying to fly higher

than their enemies became hypoxic (without cabin pressurization), lost consciousness, and crashed. Physicist Glen Millikan (1906–1947) developed oximetry in 1940 as a pilot warning device, but the technology became practical only when pulse oximetry was introduced in approximately 1980. The polio epidemics drove the development of artificial ventilation, with the need for carbon dioxide analysis to guide the ventilation of a paralyzed patient. The mid-20th-century advances in the use of hypothermia and cardiopulmonary bypass necessitated frequent monitoring of oxygenation and acid–base status.53 Severinghaus built a cuvette for the carbon dioxide electrode and mounted it in a 37◦ C water bath. His modifications of Stow’s invention cut analysis time from an hour to two minutes. Clark had built a successful bubble-type blood oxygenator to perfuse livers.54 To measure PO2 in the oxygenator, he turned to polarography. In 1954, Clark made an electrically insulated polarographic sensor with cathode and reference electrode combined, permitting it to work in either air or liquid. With Clark’s approval, Severinghaus used his electrode and his modification of Stow’s carbon dioxide electrodes in a blood gas analyzer. Severinghaus displayed the first blood PO2 and PCO2 analyzer at the fall American Society of Anesthesiologists meeting in 1957.55 The addition of a pH electrode completed the modern arterial blood analysis device. In the 1960s, with the advent of oxygen therapy and positive pressure ventilation of premature infants, it became apparent that excessive oxygenation was associated with blindness. Transcutaneous blood gas monitoring was developed primarily to avoid oxygen-induced retinopathy of prematurity. A skin surface oxygen electrode heated to 44◦ C accurately monitored PaO2 .56 Severinghaus further developed a transcutaneous PCO2 electrode57 and combined oxygen and carbon dioxide electrodes under a single membrane.58

Neuromuscular monitoring At the time when d-tubocurarine (1942), alcuronium (1964), and pancuronium (1967) were the staple relaxants, Christie and Churchill-Davidson59 and Katz60 first popularized the use of peripheral nerve stimulation in the mid-1960s (the BlockAid monitor) to evaluate neuromuscular function. This device applied a twitch (every four seconds) or tetanic stimulation (30 Hz on demand). These investigators popularized the observation and recording of adductor responses from the thumb, elicited via the ulnar nerve at the wrist.60 Shortly thereafter, Ali and others (1971)61 introduced train-of-four (TOF) stimulation, and Lee (1975)62 further popularized this technique by quantifying and correlating depth of blockade (percent twitch inhibition) according to the TOF count. The TOF technique has remained the most useful method of evaluation of neuromuscular function in clinical anesthesia practice for more than thirty years because of its simplicity and ease of evaluation and because the stimulus pattern creates its own internal standard each time the response is evaluated; that is, the strength of the fourth response is simply compared with

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that of the first without the need for establishment of a baseline prior to the administration of neuromuscular blocking drugs.63

Safety-driven monitoring standards As recounted by Ellison Pierce, the latest historical drivers of improvements in anesthesia monitoring were a combination of media attention to anesthetic deaths and a malpractice insurance rate crisis of the 1970s and 1980s.64 The field of anesthesia safety research was advanced in 1978 with the publication of Jeffrey Cooper’s first paper describing critical incident analysis applied to anesthesia.65 Cooper stated, “Factors associated with anesthetists and/or factors that may have predisposed anesthetists to err have, with a few exceptions, not been previously analyzed. Furthermore, no study has focused on the process of error – its causes, the circumstances that surround it, or its association with specific procedures, devices, etc. – regardless of final outcome.” Data for this first critical incident technique study were obtained from 47 interviews of staff and resident anesthesiologists. In a follow-up paper published in 1984, the database was enlarged to include 139 practitioners and 1089 descriptions of preventable critical incidents.66 Cooper proposed corrective strategies to lessen the likelihood of an incident occurring, including using appropriate monitoring instrumentation and vigilance.67 Major mortality studies have come from the United Kingdom, where Lunn and associates established a confidential, anonymous system to report anesthesia deaths associated with surgery. Their initial report was published in 1982, and anesthesia was considered partly or totally causative of mortality in one or two cases per 10,000 and to be totally causative in nearly 1 per 10,000. Their monitoring-related findings were that that large numbers of patients did not have blood pressure recorded intraoperatively and did not have intraoperative monitoring with the electrocardiogram.68 The Closed Claims Project of the American Society of Anesthesiologists (ASA) found that adverse respiratory events constituted the single largest class of injury, some 35 percent of the total.69 The first three mechanisms of adverse respiratory events were inadequate ventilation (38%), esophageal intubation (18%), and difficult intubation (17%), and the majority of respiratory claims were lodged before widespread adoption of pulse oximetry and capnography. The reviewers concluded that better monitoring would have prevented adverse outcomes in three-quarters of the respiratory claims, compared with only around 10 percent in the nonrespiratory cases. There is indirect evidence that the advent of ASA basic monitoring standards has diminished the incidence of adverse respiratory events in anesthesia. Eichhorn reviewed 1 million anesthetics administered to ASA physical status 1 and 2 patients at the various Harvard hospitals between 1976 and 1985, and noted 11 major intraoperative anesthesia accidents (2 cardiac arrests, 4 cases of severe brain damage, and 5 deaths).70 The most common cause (7 of 11) was an unrecognized lack of ven-

6

tilation. He concluded that these seven, as well as one other, in which oxygen was discontinued inadvertently, would have been prevented by “safety monitoring.” Of the next 300,000 anesthetics after the institution of the Harvard capnography and pulse oximetry monitoring standards in 1985, there were no major preventable intraoperative anesthesia injuries. The evidence-based monitoring standards and guidelines that emerged in the 1980s and 1990s have changed the practice of anesthesia and evolved over time. The ASA and peer organizations embraced evidence-based standards and practice parameters related to basic monitoring standards, transesophageal echocardiography, and pulmonary artery catheterization (http://www.asahq.org/publicationsAndServices/sgstoc. htm, accessed February 7, 2011). In conclusion, the history of anesthesia monitoring is a fascinating prelude to the remainder of this text. A remarkable group of perioperative physicians who were dedicated to improving patient outcomes persevered to advance the specialty, despite resistance from peers who did not share their vision. The gradual advance in the quality and sophistication of instrumentation and the regression of clinician observations of physical signs is another theme that is remarked on by every chronicler of anesthesia history. The recent decades have also brought the rise of standards in monitoring practice. The history of anesthesia clearly shows how safer anesthesia practices have arisen through improved patient monitoring. The lesson to be taken from this chapter is that we still have the capacity for further improvements in perioperative patient safety, and that we will remember most clearly those perioperative physicians who advance that goal.

Acknowledgments The author is indebted to Selma Harrison Calmes, M.D., Lydia A. Conlay, M.D., Ph.D., Doris K. Cope, M.D, James C. Erickson III, M. Ellison C. Pierce, Jr., M.D., John Severinghaus, M.D., and George Silvay, whose writings served as the source material for this chapter. Additionally, the staff of the Wood Library–Museum of Anesthesiology, Park Ridge, IL, were instrumental in providing research and support.

References 1. Harvey W. De Motu Cordis (translated by Chauncey Leake), Tercentenary ed. Springfield, IL: Charles C. Thomas, 1928. 2. Hales S. An account of some hydraulic and hydrostatical experiments made on the blood and blood vessels of animals. In Willus FA, Keyes RE, eds. Cardiac Classics. St. Louis: Mosby, 1941;I:131–155. 3. Bernard C. Lec¸on sur la chaleur animale. Paris: Libraire J-M. Bailliere et Fils, 1876. 4. Snow J. On the Inhalation of the Vapour of Ether in Surgical Operations. London: John Churchill, 1847; reproduced by Lea & Febiger, Philadelphia, 1959. 5. Syme WS. The Scottish chloroform legend – Syme and Simpson as practical anesthetists. In Essays on the First Hundred Years of Anesthesia. Huntington, NY: Robert Kreiger, 1972, Chapter 8.

Chapter 1 – The History of Anesthesia and Perioperative Monitoring

6. Duncum B. The Development of Inhalation Anaesthesia. Part 9: The beginnings of modern anaesthesia. Chapter 18: The jubilee of anaesthesia. Geoffrey Cumberlege, London: Oxford University Press. 1947:537–540. 7. Clover JT. On an Apparatus for Administering Nitrous Oxide Gas and Ether, Singly or Combined. Br Med J 1876;2(Issue 811):74–75 (Published 15 July 1876). 8. Simpson WG, ed. Works of Sir J. J. Simpson. New York: Appleton & Co., 1872. 9. Sreevastava DK, Mohan CVR. First lady physician anaesthesiologist in the world: an Indian. Indian J Anaesth 2006;50:103. 10. Pierce EC, Jr. Does monitoring have an effect on patient safety? Monitoring instruments have significantly reduced anesthetic mishaps. J Clin Monit 1988;4(2):111–114. 11. Momin Ali, Asrit Ramachari. About the participants in the Hyderabad Choloform Commissions. In Fink BR, Morris LE, Stephen CR (eds). The History of Anesthesia: Third International Symposium. Wood Library Museum of Anaesthesiology, Illinois. 1992; 28–31. 12. Kirk R. On auscultation of the heart during chloroform narcosis. Br Med J 1896;2:1704–1706. 13. Teter CK. Thirteen thousand administrations of nitrous oxid with oxygen as an anesthetic. JAMA 1909;53:448–454. 14. Cushing H. Technical methods of performing certain cranial operations. Surg Gynecol Obstet 1908;VI:227–234. 15. Solis-Cohen S. Exhibition of an oesophageal stethoscope, with remarks on intrathoracic auscultation. Trans Cell Physicians Philadelphia 1893;3.5 XV:218–221. 16. Fink, BR. Times of the Signs, The Origins of Charting, The History of Anesthesia, 3rd International Symposium Proceedings. B.R. Fink, L.E. Morris, C.R. Stephen, eds. Chicago: Wood Library-Museum, 1992. 17. Cushing HW. On the avoidance of shock in major amputations by cocainization of large nerve trunks preliminary to their diversion, with observations on blood-pressure changes in surgical cases. Ann Surg 1902;36:321–343. 18. Major RH. The history of taking the blood pressure. Ann Medical Hist. 1930;2:47–55. 19. Riva-Rocci S. A new sphygmomanometer. In Faulconer A, Keyes TE, eds. Foundations of Anesthesiology. Springfield, IL: Charles C. Thomas, 1965;2:1043–1075. 20. Cushing HW. On routine determinations of arterial tension in operating room and clinic. Boston Med Surg J 1903;148: 250–256. 21. Korotkoff NS. On the subject of methods of determining blood pressure. Bull Imp Mel Med Acad St. Petersburg 1905; 11:365. 22. von Recklinghausen H. Ueber Blutdruckmessung bein menschen. Arch F exp Path U Pharmakol 1901: 46:78. 23. Von Recklinghausen H. Neue Wege zur Blutdruckmessung. Berlin: Springer-Verlag, 1931. 24. Kazamias TM, Gander MP, Franklin DL, Ross J Jr. Blood pressure measurement with Doppler unltrasonic flowmeter. J Appl Physiol 1971;30:585–588. 25. Kirby RR, Kemmerer WT, Morgan JL. Transcutaneous measurement of blood pressure. Anesthesiology 1969;31: 86–89. 26. Zahed B, Sadove MS, Hatano S, Wu HH. Comparison of automated Doppler ultrasound and Korotkoff measurements of blood pressure of children. Anesth Analg 1971;50:699–704. 27. Silas JH, Barker AT, Ramsey LE. Clinical evaluation of Dinamap 845 automated blood pressure recorder. Br Heart J 1980;43: 202–205.

28. Gillespie NA. The signs of anesthesia. Anesth Analg. 1943;22:275–282. 29. Calmes SA. Arthur Guedel, M.D. and the eye signs of anesthesia. ASA Newsletter, September 2002. https://www.asahq.org/ Newsletters/2002/9 02/feature5.htm (accessed May 25, 2009). 30. Courington FW, Calverley RK. Anesthesia on the western front: the Anglo-American experience of World War I. Anesthesiology 1986;65:642–653. 31. Poiseuille JLM. R´echerches sur la force du Coeur aortique. Arch Gen Med 1828;18:550–555. 32. Ludwig C. Beitrage zur kenntniss des einflussen der respiratiores bewegungen auf den blut auf in aortensysteme. Muller’s Arch Anat 1847;240–302. 33. Peterson LH, Dripps RD, Risman GC. A method for recording the arterial pressure pulse and blood pressure in man. Am Heart J 1949;37:771–782. 34. Heard JD, Strauss AE. A report on the electrocardiographic study of two cases of nodal rhythm exhibiting R-P intervals. Am J Med Soc 1918;75:238–251. 35. Levine SA. Acute cardiac upsets occurring during or following surgical operations. JAMA 1920;75:795–799. 36. Lennox WG, Graves RC, Levine SA. An electrocardiographic study of fifty patients during operation. Arch Int Med 1922;30:57–72. 37. Maher CJ, Crittenden PJ, Shapiro PT. Electrocardiography study of viscerocardiac reflexes during major operations. Am Heart J 1934;9:664–676. 38. Kurtz CM, Bennet JH, Shapiro HH. Electrocardiographic studies during surgical anesthesia. JAMA 1936;106:434–441. 39. Feil H, Rossman PL. Electrocardiographic observations in cardiac surgery. Ann Intern Med 1939;13:402–414. 40. Ziegler RF. Cardiac mechanism during anesthesia and operation in patients with congenital heart disease and cyanosis. Bull Johns Hopkins Hosp 1948;83:237–71. 41. Himmelstein A, Scheiner M. The cardiotachoscope. Anesthesiology 1952;13:62–64. 42. Cannard TH, Dripps RD, Helwig J Jr, Zinsser HF. The electrocardiogram during anesthesia and surgery. Anesthesiology 1960; 21:194–202. 43. Russell PH, Coakley CS. Electrocardiographic observation in the operating room. Anesth Analg 1969;48:474–488. 44. Kaplan JA, King SB. The precordial electrocardiographic lead V5 in patients who have coronary artery disease. Anesthesiology 1976;45:570–574. 45. Blackburn H, Taylor HL, Okamoto N, Rautaharju P, Mitchell PL, Kerkhof AC. Standardization of the exercise electrocardiogram. A systematic comparison of chest lead configuration employed for monitoring during exercise. In Karvaner MJ, Barry AD, eds. Physical Activity and the Heart. Springfield, IL: Charles C. Thomas, 1967; 101–133. 46. Kaplan JA. Electrocardiographic monitoring. In Kaplan, JA, ed. Cardiac Anesthesia. New York: Grune and Stratton, 1979; 149–151. 47. Forssmann W. Die Sondierung de rechten Herzens Klin Wochenschr 1929; 8:2085–2087. 48. Klein O. Zur Bestimmung de zerkulatorischen minutens. Volumen nach dem Fickschen Prinzip. Munch Med Wochenschr 1930; 77:1311. 49. Cournand AF. Measurement of cardiac output in man using the technique of catheterization of the right auricle. J Clin Invest 1945;24:105–116. 50. Dexter L, Haynes FW, Burwell CS, Eppinger EC, Sagerson RP, Evans JM. Studies of congenital heart disease: II. The pressure and

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51.

52.

53.

54. 55. 56.

57.

58.

59.

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oxygen content of blood in the right auricle, right ventricle and pulmonary artery in control patients, with observations on the oxygen saturation and source of pulmonary “capillary” blood. J Clin Invest 1947;26:554–560. Lagerlof H, Werko L. Studies on the circulation of blood in man. VI. The pulmonary capillary venous pressure pulse in man. Scand J Clin Lab Invest 1949;1:147–161. Swan HJC, Ganz W, Forrester J, Marcus H, Daimond G, Chonette D. Catheterization of the heart in man with use of a flow directed balloon-tipped catheter. N Engl J Med 1970;283:447–451. Severinghaus JW. Gadgeteering for health care: The John W. Severinghaus Lecture on Translational Science. Anesthesiology 2009;110:721–728. Clark LC Jr, Gollan F, Gupta VB. The oxygenation of blood by gas dispersion. Science 1950;111:85–87. Severinghaus JW, Bradley AF. Electrodes for blood pO2 and pCO2 determination. J Appl Physiol 1958;13:515–520. Severinghaus JW, Peabody JL, Thunstrom A, Eberhard P, Zappia E, eds. Workshop on methodologic aspects of transcutaneous blood gas analysis. Acta Anaesthesiol Scand Suppl 1978;68:1–144. Severinghaus JW. A combined transcutaneous PO2 -PCO2 electrode with electrochemical HCO3 -stabilization. J Appl Physiol 1981;51:1027–32. Palmisano BW, Severinghaus JW. Clinical accuracy of a combined transcutaneous PO2 -PCO2 electrode. Crit Care Med 1984;12:276. Christie TH, Churchill-Davidson HC. The St. Thomas’s Hospital nerve stimulator in the diagnosis of prolonged apnoea. Lancet 1958;1:776.

60. Katz RL. A nerve stimulator for the continuous monitoring of muscle relaxant action. Anesthesiology 1965;26:832. 61. Ali HH, Utting JE, Gray C. Quantitative assessment of residual antidepolarizing block (part II). Br J Anaesth. 1971; 3:478. 62. Lee CM. Train-of-4 quantitation of competitive neuromuscular block. Anesth Analg 1975;54:649. 63. Savarese JJ. Monitoring of neuromuscular function: past, present and future. ASA Newsletter, September 2002. https://www.asahq. org/Newsletters/2002/9 02/feature6.htm (accessed May 25, 2009) 64. Eichhorn JH. Prevention of intraoperative anesthesia accidents and related severe injury through safety monitoring. Anesthesiology 1989;70:572–577. 64. Cooper JB, Newbower RS, Long CD, McPeek B. Preventable anesthesia mishaps: a study of human factors. Anesthesiology 1978;49:399–406. 66. Cooper JB, Newbower RS, Kitz RJ. An analysis of major errors and equipment failures in anesthesia management: considerations for prevention and detection. Anesthesiology 1984;60:34–42. 67. Cooper JB. Toward prevention of anesthetic mishaps. In Pierce EC Jr, Cooper JB, eds. Analysis of Anesthetic Mishaps. Boston: Little, Brown, 1984:167–183. 68. Lunn JN, Mushin WW. Mortality Associated with Anaesthesia. London: Nuffield Provincial Hospitals Trust, 1982. 69. Caplan RA, Posner KL, Ward RJ, Cheney FW. Adverse respiratory events in anesthesia: A closed claims analysis. Anesthesiology 1990;72:828–833. 70. Eichhorn JH. Prevention of intraoperative anesthesia accidents and related severe injury through safety monitoring. Anesthesiology 1989;70:572–577.

Chapter

2

Medicolegal implications of monitoring Jeffrey M. Feldman

Introduction If you have never received a letter with the return address of an unknown law firm, consider yourself lucky. In the case of a malpractice proceeding, you will open the letter and typically find your name in a long list of defendants. Sometimes the letter is anticipated, but often, the precipitating events occurred so long ago that the details are difficult to recall. Whatever the circumstances, a malpractice suit unleashes a sequence of events with an unpredictable outcome. The trial venue, the quality of the attorneys, the members of the jury, the expert witnesses involved, the ability of the plaintiff to engender sympathy, the perceived credibility of the defendant, and the quality of the documentation all play a role in the ultimate outcome. The plaintiff ’s attorney will leave no stone unturned in building the case for malpractice. Because physiologic monitoring is essential to safe patient care, the plaintiff ’s attorney is likely to scrutinize how the patient was monitored in building the case. The intent of this chapter is to explore the ways in which physiologic monitoring and exposure to malpractice liability are related. The intent is not to offer a comprehensive discussion of the nuances of malpractice liability. If you are named in a malpractice suit, there is no better resource than a skilled defense attorney. In a chapter titled “Medical Liability and the Culture of Technology,” Jacobsen argues, “The history of medical liability is a struggle between technological advances and injuries suffered when those advances fail.”1 He goes on to observe that technical advances empower physicians to tackle ever more complex and challenging medical problems with the attendant increased risks. In some cases, the outcome is a return to the previous state of health, but that is not always the case. The public, on the other hand, demands – and has come to expect – perfect outcomes. Although a physician may clearly understand that a less-than-perfect outcome is much better than even more severe disability or death, the patient perceives only the loss of his or her health. Physiologic monitoring has facilitated increasingly complex surgical procedures for sicker patients. Even the most confident clinician would be unlikely to attempt to provide anesthesia for liver transplantation using just a finger on the pulse. The most sophisticated monitoring, however, cannot prevent undesired outcomes in sick patients undergoing complex procedures and the resulting exposure to malpractice suits.

Although the proliferation of technology can increase the potential for malpractice liability, Jacobsen recognizes that the specialty of anesthesiology provides one example in which technology, and patient monitoring in particular, has actually reduced malpractice liability by reducing the risk of serious injury. For a number of years, anesthesiology ranked at the top of the medical specialties in malpractice claims and the severity of patient injury. In 1986, the Harvard Medical School Department of Anesthesia adopted a minimum standard for patient monitoring during anesthesia.2 This standard included provisions for monitoring ventilation, preferably by capnography. Interestingly, pulse oximetry, which had only recently been introduced, was advocated as a means to monitor the circulation, not oxygenation. The primary goal of the Harvard standard was to improve patient safety by reducing adverse events, with a secondary goal of reducing malpractice claims. Malpractice insurance carriers became convinced of the value of these guidelines to mitigate malpractice exposure and, in an effort to catalyze more widespread adoption, offered to reduce premiums to practices that adhered to the monitoring guidelines. The result was a significant reduction in the number and severity of claims against anesthesiologists.3 A review of 1175 closed malpractice claims filed between 1974 and 1988 underscores the potential for physiologic monitoring to reduce malpractice claims. The reviewers determined that one-third of the injuries could have been prevented by the use of monitoring devices, most notably pulse oximetry and capnometry.4 Establishing monitoring standards was facilitated by the development of monitoring devices that were easy to use and cost-effective. The resulting outcome clearly established the relationship between physiologic monitoring and patient safety. The motivation for these efforts was to reduce the risk of patient injury. The financial realities of the malpractice system created the business case, as avoiding even one wrongful death or hypoxic injury suit would pay for multiple patient monitors. Risk management strategies typically focus on adherence to the standard of care, the importance of documentation, and the patient–physician relationship. Monitoring patients appropriately reduces the risk of significant injury and is therefore an important part of risk management in anesthesia. As a result of the Harvard experience, the American Society of Anesthesiologists (ASA) established a standard for anesthetic monitoring.

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It is notable that the ASA has chosen to include the word “standard” in the title of this document, which establishes the content to indicate the standard of care.∗ As we will see, this monitoring standard is the most unambiguous evidence that can be presented in court for the standard of care because it does not require the opinion of an expert witness. Furthermore, there is good evidence from the ASA closed-claims database that when adherence to a standard of care can be demonstrated, there is a reduced chance of payment for a malpractice claim.5 To better understand the importance of the standard of care, consider the elements of proof that are required in a malpractice proceeding.

Burden of proof Although the outcome of a malpractice suit can sometimes seem capricious, the burden of proof that must be satisfied by the plaintiff ’s attorney is well defined. Understanding the burden of proof is a useful foundation for evaluating the role of any aspect of care that is used to build a case for malpractice. In the broad sense, health care malpractice liability arises from five areas of exposure:6 r Professional negligence (substandard care delivery) r Intentional misconduct r Breach of a therapeutic promise (breach of contract) r Patient injury from dangerous treatment-related activities, regardless of fault (strict liability) r Patient injury from dangerous devices (product liability) Of these areas of exposure, professional negligence is the most common basis for suit against an individual health care provider. Most of the discussion in this chapter focuses on the role of physiologic monitoring in establishing a case for negligence against a health care provider. Physiologic monitors can be involved in a suit related to strict or product liability. In the latter case, the liability suit would typically be directed toward the manufacturer, and debate would ensue about whether it was the device or failure to use it correctly that caused the injury. Negligence is defined as “conduct which falls below the standard established by law for the protection of others against unreasonable risk of harm.”7 When professional negligence is considered, the “standard” by which the care is measured is considered to be the minimally acceptable practice. Practitioners accused of negligence in a malpractice case are judged not by the standard set by the most skilled practitioner, but by the standard set by an ordinary practitioner under usual circumstances. The role of the expert witness is therefore to articulate not how he or she personally would have treated the patient, but what is generally considered to be the minimal safe practice standard. Different rules can be applied to defining the ∗

10

The ASA also issues “Guidelines” and “Statements” that are intended to provide information about practice decisions but are not considered a standard of care. The distinction is important in a malpractice proceeding. For more information, see http://www.asahq.org/publicationsAndServices/ sgstoc.htm.

minimal safe practice standard. In some cases, the professional is held to the standard in his or her geographic practice area so, for example, a rural physician in a community hospital is not held to the same standard as a physician with the resources of a tertiary-care urban hospital. For individual specialties, the standard could be applied to a reasonably prudent professional in the same specialty. Negligent acts can be acts of commission or omission. In the former case, the liable party must do something that, under similar circumstances, a reasonably prudent professional would have done differently or not at all. An act of omission is the failure to do something that a reasonably prudent professional would have done under the same circumstances. An act of commission in patient monitoring, for example, would involve using a monitoring device that exposes a patient to injury when using that device would not be considered standard of care. An act of omission in patient monitoring would involve failing to use a monitoring modality that is considered the minimal safe practice. The terminology “reasonably prudent professional” is an attempt to create an objective standard for evaluating a person’s actions. In the case of an anesthesia provider, the “reasonably prudent” definition would indicate an individual who is trained and licensed in accordance with applicable laws and professional standards. The failure to follow indicated monitoring standards is not in itself sufficient proof of negligence. The plaintiff’s attorney has the burden to prove the following four elements:8 r The professional had a duty to care for the patient. r The professional breached the duty to care for the patient by providing substandard care. r The injury suffered by the patient was caused by the breach of duty. r The damages to the patient are compensable. Of these four elements, the second and third can be related to the manner in which a physiologic monitor is used. Using a device that may cause injury when the device is not indicated, or failing to use a device when it is indicated, are examples of substandard care absent a compelling explanation by the provider. Other examples would include pulmonary artery rupture from placing a pulmonary artery catheter that is not indicated, or hypoxic injury when a pulse oximeter is not used. The burden of proof also requires that the injury suffered by the patient be related to the breach of duty to provide care consistent with the prevailing standard. In the strictest definition, one would need to establish a clear link between the aspect(s) of the care that are substandard and the injury suffered by the plaintiff. Given the uncertainties of medicine, it is not always possible to establish direct causation for a particular injury. The plaintiff ’s attorney may argue that breach of duty need not be proven based on the principle of res ipsa loquitur, or “the thing speaks for itself.” This burden of proof is not as rigorous as in the case of strict professional negligence, as a causative link between the care lapse and the injury is not required. To argue

Chapter 2 – Medicolegal Implications of Monitoring

for liability on the basis of res ipsa loquitur, the attorney must prove that r The injuries suffered by the plaintiff would not normally occur in the absence of negligence; r The defendant(s) had both the ability and the duty to prevent such injuries; and r The plaintiff did not contribute to causing his or her own injury. Although the burden of proof for professional negligence is clearly established, differences of opinion between expert witnesses are typical. In a review of 103 closed anesthesia malpractice claims, independent paired reviewers disagreed about the appropriateness of care in 38 percent of the cases using the standard of a reasonable and prudent anesthesia practitioner.9 These findings underscore the fact that the standard of care is a matter of opinion, and both plaintiffs and defense attorneys are likely to find well-intentioned credible experts to support their views. The ultimate decision of a lay jury can be swayed by many factors. As we will see, failure to monitor can cast a very negative light on the health care practitioner, and if the patient has suffered injury, the jury is likely to provide compensation. Under the principle of res ipsa loquitur, linking the injury directly to the failure to monitor may not be needed to convince the jury to find for the defendant.

Monitoring standards It is 2 AM. A 24-year-old patient is on the way to the operating room for an emergency appendectomy. You check the anesthesia machine and find that the inspired oxygen monitor cannot be calibrated and does not provide a reading. Do you proceed with the case? When it comes to defining the standard of care with regard to physiologic monitoring, we are fortunate to have the ASA Standards for Basic Anesthetic Monitoring.10 As noted previously, that document clearly defines the recognized minimum standard for patient monitoring, inclusive of all regional, general, and monitored-care anesthetics. The standard guidelines are divided broadly into two categories. The first emphasizes that the anesthesia provider be physically present at all times to ensure adequate patient monitoring. The second category requires, “During all anesthetics, the patient’s oxygenation, ventilation, circulation and temperature shall be continually evaluated.” For the most part, these standards are self-explanatory. The language in the standard is carefully chosen in an attempt to limit malpractice exposure when adherence to the standard either is impractical or would present a greater risk to the patient. For virtually all the recommended monitoring strategies, there is an opportunity to waive a specific requirement under extenuating circumstances. The standard emphasizes the importance, however, of documenting the reasons for waiving the requirement in the patient’s medical record.

One can be certain that in the event of a patient injury that could even remotely be related to physiologic monitoring, adherence to the ASA Standards for Basic Anesthetic Monitoring will be scrutinized by the plaintiff ’s attorney. Any variation from this standard will be used to identify a cause for the injury and to impugn the quality of care rendered by the anesthesia provider. An interesting example of this scenario has been reported by Vigoda and Lubarsky.11 The report describes the case of a 58-year-old male who underwent a craniotomy for a brain tumor while in the sitting position and suffered newonset quadriplegia after the procedure. During the case, the Standards for Basic Anesthesia Monitoring were followed and, in particular, arterial pressure monitoring was performed using an intraarterial catheter for continuous measurement. The case involved the use of an anesthesia information management system (AIMS) to acquire data from the monitors and create the anesthetic record. During the procedure, there was a 93-minute period of time during which the data from the arterial pressure monitor did not appear on the automated anesthesia record. It turned out that there was a problem with the cable connecting the physiologic monitor to the AIMS, so blood pressure data were not transferred to the recordkeeper. The providers caring for the patient did not notice this problem, as they were able to follow the blood pressure on the display of the physiologic monitor, and the blood pressure data on the AIMS display were covered by an informational window. A malpractice claim was filed and ultimately settled during the trial phase. Although the patient’s injury was not clearly linked to substandard monitoring, conformance with the standard of care was not documented by the record, and successful defense became unlikely. This case report raises another interesting consideration regarding the use of an AIMS and liability exposure related to monitoring standards. In contrast to a paper record, the AIMS provides a continuous electronic record of monitored information. In addition to the paper record printed at the conclusion of a case, all the data are time-stamped and archived to an electronic database. Both the paper record and the electronic database are discoverable and will provide the most authoritative information available to a jury to decide how a patient was monitored. The design of the AIMS used by Vigoda and Lubarsky has been changed, as a consequence of their experience, to alert the provider when a monitoring failure has occurred. Anyone using an AIMS would do well to review the case report and understand how the system will document conformance with minimal monitoring standards. Given these considerations, in general, one should not render anesthetic care unless conformance with the standards for basic monitoring can be met. Exceptions to this rule involve emergency procedures when delaying the start of care would increase the risk to the patient. If the scenario of the appendectomy was, instead, that of a trauma victim who is rushed from the emergency department to the OR for a lifesaving surgical intervention, it would not be advisable to delay the procedure to troubleshoot an oxygen monitor. It is important, however, to document as soon as possible why the procedure started

11

Monitoring in Anesthesia and Perioperative Care

without that monitoring modality, and to make every effort to institute the ability to monitor that parameter.

Monitoring beyond the standards The ASA Standards for Basic Anesthesia Monitoring should be followed for every anesthetic, but additional monitoring is often used. Additional monitored parameters include cardiac output, mixed venous oxygen saturation, processed electroencephalography, evoked potentials, and echocardiography. Although these monitoring modalities are not included in the minimum monitoring standard, there is significant potential for the use of these monitors to be scrutinized in the event of a malpractice suit. This is especially true when one considers that these additional devices are typically used for patients and procedures where there is an increased risk of an untoward outcome. Clearly, if the risk of a bad outcome is increased, then the risk of a malpractice suit is increased as well. Unfortunately, both using a monitor and failing to use a monitor can result in liability exposure. A 35-year-old healthy male patient is scheduled for an open removal of a renal staghorn calculus and possible nephrectomy. After induction of general anesthesia, a central venous catheter is placed; shortly thereafter, the patient becomes hypotensive, suffers a cardiac arrest, and cannot be resuscitated. The postmortem examination identifies hemopericardium, with resulting cardiac tamponade, as the cause of death. Complications related to central venous catheter placement are well recognized. In 2004, Domino and coworkers used the ASA closed-claims database to evaluate claims related to central venous catheter placement. They identified 110 claims related to central venous catheters with a greater severity of injury and proportion of death than the other claims in the database. Cardiac tamponade, hemothorax, and pulmonary artery rupture were the common causes of death.12 In the case example, there is little doubt that central venous catheter placement led to the patient’s demise. From a malpractice perspective, one question that will be raised is whether central venous catheter placement was indicated in this case. In the absence of a reference for the standard of care, the professional is in the position of having to justify the risk to the patient based on the potential benefit. Secondarily, plaintiff ’s attorneys could question the experience of the person placing the catheter and the method of placement. Ultrasound guidance has proven to be useful for central catheter placement (see Chapter 12). Although it is useful for directing needle placement, ultrasound has not been shown to prevent the serious complications that can result from central catheter placement, especially those that can occur after finding the vein. Well-considered differences of opinion on the standard of care will exist when attempting to address the questions raised by this case scenario.

12

Although a monitor may not be considered a “standard,” using that monitor could be considered part of the duty to use reasonable care to protect a patient from harm.13 Adopting a monitor into clinical practice is an implicit statement that it is useful for patient care. Scientific documentation linking a monitor to improved outcome may not exist, but expert witnesses can use evidence from the literature that these monitors reduce the risk of serious complications and are considered part of the reasonable duty to protect a patient from harm. A 60-year-old man with a history of peripheral vascular disease is scheduled for a lower-extremity arterial bypass. General anesthesia is administered, including the use of a muscle relaxant. During the surgical preparation, the patient’s arterial blood pressure is 100/50 and the concentration of inhaled anesthetic is minimized. After awakening, the patient reports recall of the surgical preparation and the pain from the incision, including the inability to move or talk. Existing literature suggests that the incidence of awareness during general anesthesia may be as high as 0.2 percent, or up to 26,000 occurrences per year in the United States alone.14 Patients who experience awareness may be left with a posttraumatic stress-like disorder and permanent psychologic impairment. There is a high likelihood, therefore, that an incident of awareness will lead to a malpractice suit. The ASA Closed Claims project has documented 56 claims for recall during general anesthesia between 1990 and 2006, although this number likely underrepresents the total number of cases. Interestingly, payment was made in just 52 percent of the claims, suggesting that the burden of proof can be difficult. A large number of awareness claims were not associated with any one single factor, but “there were indications that lower doses of anesthetic agents may be associated with recall.”15 How would monitoring modalities intended to assess the risk of awareness be viewed in a malpractice proceeding? Could it be considered negligence if one of these monitors was not used and the patient suffered intraoperative recall? Monitoring exhaled anesthetic agent concentration is not considered a monitoring standard but is certainly widely used, and the information is often recorded to a handwritten record or AIMS. A variety of neurophysiologic monitors are available that are designed to help the clinician assess anesthetic depth (see Chapter 18). Neither anesthetic agent monitors nor neurophysiologic monitors are included in the ASA basic monitoring standards. Nevertheless, there is an accumulating body of literature that could be used to argue for the use of these monitors, especially in selected “high-risk” patients. In 2004, the Joint Commission (TJC; formerly known as the Joint Commission on the Accreditation of Healthcare Organizations, abbreviated as JCAHO) issued a sentinel event alert on Preventing and Managing the Impact of Anesthesia Awareness. In this alert, TJC recommended “[the] effective application of available anesthesia monitoring techniques” as a preventive strategy.16 In that

Chapter 2 – Medicolegal Implications of Monitoring

same year, the ASA published a practice advisory on Intraoperative Awareness and Brain Function Monitoring.17 The report specifically states that the practice advisory is not intended as a standard, guideline, or absolute requirement. With regard to preventing awareness, the advisory states that “brain function monitoring is not routinely indicated for patients undergoing general anesthesia, either to reduce the frequency of intraoperative awareness or to monitor depth of anesthesia,” and further stated that “the decision to use a brain function monitor should be made on a case-by-case basis by the individual practitioner for selected patients.” The practice advisory does advocate for multimodality monitoring (including anesthetic agent monitoring) to minimize the occurrence of awareness and does state that the use of a muscle relaxant “adds additional importance to the use of monitoring methods that assure the adequate delivery of anesthesia.” Whether a jury would consider an anesthetic agent or depth-of-anesthesia monitor to be consistent with minimally acceptable practice will depend on the arguments of the attorneys and the testimony of expert witnesses. Even though awareness monitoring is not included in the ASA Basic Anesthesia Monitoring Standards, the language in the practice advisory suggests that selected high-risk patients would benefit from monitoring for awareness. Regardless of what monitoring strategy is used, whenever a patient receives general anesthesia there is the potential for awareness, and the anesthesia professional should be able to articulate the strategy that was employed to prevent awareness. Patient awareness is just one of the events that has a high likelihood of resulting in a malpractice suit when monitoring beyond the basic standard can be involved. Patients with significant hemodynamic compromise (e.g., trauma patients), or patients at risk for intraoperative stroke (e.g., major vascular or neurosurgery) also have a high likelihood of poor outcome and a related increased likelihood of suit. Even though there may not be specific indications for monitoring beyond the standards defined by the ASA, there is enough literature about the potential value of advanced monitoring devices that not using these devices may be called into question. It is beyond the scope of this chapter to explore all of these potential sources of liability. Further, the indications for most advanced monitoring techniques are not so well established that one can define when and how monitoring beyond the ASA standard would be considered a community standard. Any attempt to do so would likely create literature that could be exploited by a plaintiff ’s attorney without any scientific basis.

Importance of training The evolution of physiologic monitors has led to devices that are both easy to use and reliable. Gone are the days of calibrating pressure transducers against mercury manometers. Today, most physiologic monitors need only be turned on and connected to the patient to obtain monitored information. Nevertheless, misuse of the monitor or the information from

the device can be the basis for malpractice liability related to negligence or strict liability. A 32-year-old woman was admitted to the intensive care unit in a coma following closed head trauma. At the change of the nursing shift, the intracranial pressure (ICP) transducer is found to have been affixed 15 centimeters above the zero point. This error occurred several hours earlier during adjustment of the height of the bed as the patient was turned for decubitus ulcer prevention. The zero is reestablished and the ICP measurement of 12 cmH2 O, which had been stable for the last six hours, is now 27 cmH2 O. Measures to reduce ICP are instituted. The patient is left with significant neurologic injury. Monitors that measure pressure are likely to provide misleading or incorrect information if they are used improperly. Even though modern transducers do not require calibration, they all require establishing a zero reference point for pressure measurement. The anatomical relationship of this reference point to the patient must be carefully established and maintained to prevent erroneous readings that can easily be clinically significant. In the case of an arterial pressure transducer, there is the potential for falsely high or falsely low measurements if the transducer is too low or too high, respectively, relative to the heart or brain. In the case of central venous pressure or ICP monitors, the location of the zero point is even more critical. Because the absolute values of those pressure measurements are relatively low, small errors in the location of the transducer relative to the zero point can have a significant impact on the monitored information. Given the severity of the injury in patients who require ICP monitoring, undesired outcomes are common, with the corresponding increased risk of a malpractice suit. Providers caring for these patients must understand the principles of pressure measurement, carefully locate the zero reference point for pressure measurement, and be sure to maintain accurate monitoring over time. Mounting transducers to the patient or the patient’s bed is useful for preventing the problem of moving the patient relative to the zero reference of the transducer. Even though many monitors have become easy to use and require little training, some advanced approaches to monitoring require significant training. Perhaps the most notable example relevant to the practice of anesthesiology is transesophageal echocardiography (TEE), which is often employed during highrisk procedures involving high-acuity patients. Proper use of this monitor requires training and experience. The National Board of Echocardiography offers a certification exam for special competence in perioperative transesophageal echocardiography, which is intended to “serve the public by encouraging quality patient care in the practice of echocardiography.”18 Although certification is not required for anesthesia professionals to perform echocardiography exams, significant patient management decisions are often guided by the results of these exams. Should an untoward outcome occur that could be related

13

Monitoring in Anesthesia and Perioperative Care

to the interpretation of the TEE, the credentials of the clinician performing the TEE would almost certainly be questioned in the event of a malpractice proceeding. The existence of the certification process creates a competency standard even though it is not required for practice. Accreditation of skills related to physiologic monitoring is available only for certain devices. Documentation of training and proficiency is currently not employed in a rigorous fashion for most devices but, from a medicolegal/risk management perspective, competency documentation can only be a benefit.

Physiologic alarms – unintended consequences? The ASA Standards for Basic Anesthesia Monitoring include the recommendation for audible alarms for low inspired oxygen concentration, low arterial oxygen saturation, the absence of end-tidal carbon dioxide, and ventilator disconnection. Audible alarms were not included in the monitoring standard until the most recent revision in 2005, despite the fact that audible alarms have been a standard feature of physiologic monitors for many years. Why were audible alarms not part of the monitoring standard from the outset? Furthermore, physiologic monitors incorporate audible alarms that are tied to virtually all the parameters monitored during anesthesia. Why is the recommendation for using audible alarms during monitoring restricted to the four alarms currently mentioned in the monitoring standard? The technology for audible physiologic alarms is, for the most part, based on setting high and low thresholds for a monitored parameter, and sounding an audible tone when the actual measured value crosses that threshold (see Chapter 35). This approach is practical from an engineering perspective, but for the most part has not resulted in clinically useful alarms. In fact, this approach to alarms has resulted in a high rate of audible alarms that are clinically meaningless (false-positive alarms), and are either disabled or just add noise and distraction to the clinical environment.19 Similar to the fable attributed to Aesop, “The Boy Who Cried Wolf,” current alarms are so often meaningless that they are either disabled or do not catch the user’s attention when an important event occurs. Several strategies have been proposed to standardize and improve on clinical alarms, yet none has been adopted in any widespread fashion.20 Given the obvious shortcomings of current alarm technology, why has there been so little progress toward improving the alarms? The inadequacy of the current alarm technology and lack of progress toward improving alarms is an unintended consequence of the medicolegal protections afforded to patients. Failure to notify the user of an important physiologic change that could lead to patient injury can only open the door for product liability. From the perspective of a manufacturer, the goal in designing audible alarms is to incorporate highly sensitive alarms that will not miss any important events. The consequence of a highly sensitive alarm is a high false-alarm rate.

14

There is little or no incentive for the manufacturer to make the alarms more specific, as the cost is almost certain to be a reduced sensitivity and the potential to miss an important event. Until a manufacturer can create a competitive advantage by improving alarm technology, there is little chance that the basic technology will be improved. Fortunately, there are efforts under way to improve the clinical utility of audible alarms. Numerous strategies have been investigated that range from simple time delays to suppress alarms from transient artifacts, to multivariate statistical approaches.21 International standards efforts are focusing on tailoring alarm tones to the specific type of alarm rather than having a nonspecific tone that is related to a certain manufacturer. Given the potential costs to manufacturers of a product liability suit, there is little incentive to take any risk with new alarm algorithms that reduce the sensitivity of the alarms unless the improved specificity is clearly documented. Because new developments are unlikely to come from industry, we will be left with the unintended consequence of audible alarms that are not clinically useful unless research can lead us to improved alarm algorithms.

Conclusions As a medical specialty, anesthesiology has been a leader in establishing the connection between the appropriate use of physiologic monitors and enhanced patient safety. The ASA Standards for Basic Anesthesia Monitoring provide an unambiguous definition of the minimum standards for monitoring. These standards should be followed for every patient unless the reasons for not following the standard can be clearly documented. As sicker patients present for more complicated procedures, the risks of undesirable outcomes increase, with the consequence of greater liability exposure. When the outcome leads to a malpractice suit, reasonable expert witnesses may argue that monitoring beyond the standard would be indicated to protect a patient from harm. From a risk management perspective, it is important to be able to explain why a device that could be considered useful to protect the patient was not used, or why a device that has inherent risks was chosen. Experience has demonstrated that keeping patients safe reduces malpractice exposure and is the best risk management strategy one can employ. Proper use of physiologic monitors can help to achieve that goal.

Acknowledgment Special thanks to Teresa Salamon, CRNA, JD, of Dechert LLP in Philadelphia for her critical review of this chapter.

References 1. Jacobsen PD. Medical liability and the culture of technology. In Sage WM, Kersh R, eds. Medical Malpractice and the US Health Care System. New York: Cambridge University Press, 2006, p. 116.

Chapter 2 – Medicolegal Implications of Monitoring

2. Eichhorn JH, Cooper JB, Cullen DJ, Maier WR, Philip JH, Seeman RG. Standards for patient monitoring during anesthesia at Harvard Medical School. JAMA 1986;256:1017–1020. 3. Jacobsen PD. Medical liability and the culture of technology, p. 126. 4. Tinker JH, Dull DL, Caplan RA, Ward RJ, Cheney FW: Role of monitoring devices in prevention of anesthetic mishaps: A closed claims analysis. Anesthesiology 1989;71:541–546. 5. Cheney FW, Posner K, Caplan RA, Ward RJ. Standard of care and anesthesia liability. JAMA 1989;261:1599–1603. 6. Scott RW. Health Care Malpractice. A Primer on Legal Issues for Professionals. 2nd Ed. New York: McGraw Hill, 1999, p. 5. 7. Boumil MM, Elias CE. The Law of Medical Liability. West Publishing, St Paul, 1995. p. 24. 8. Scott RW. Health Care Malpractice, pp. 16–18. 9. Posner KL, Caplan RA, Cheney FW: Variation in expert opinion in medical malpractice review. Anesthesiology 1996;85:1049–54. 10. American Society of Anesthesiologists. ASA Basic Monitoring Standards. Amended October 25, 2005. http://www.asahq. org/publicationsAndServices/sgstoc.htm (as of 1/10/2009). 11. Vigoda MM, Lubarsky DA. Failure to recognize loss of incoming data in an anesthesia record-keeping system may have increased medical liability. Anesth Analg 2006;102:1798–802. 12. Domino KB, Bowdle TA, Posner KL, Spitellie PH, Lee LA, Cheney FW. Injuries and liability related to central vascular

13. 14.

15. 16. 17. 18. 19.

20.

21.

catheters: a closed claims analysis. Anesthesiology. 2004;100: 1411–1418. Pegalis SE. American Law of Medical Malpractice, 3d ed., vol 2. West Eagan, MN: Thomson, 2005;11:7. Sebel PS, Bowdle TA, et al. The incidence of awareness during anesthesia: a multicenter United States study. Anesth Analg 2004;99:833–9. Kent CD. Liability associated with awareness during anesthesia. ASA Newsletter 2006;70(6): 8–10. JCAHO Sentinel Alert. Preventing, and managing the impact of, anesthesia awareness. Volume 32, October 6, 2004. Practice Advisory for Intraoperative Awareness and Brain Function Monitoring. Anesthesiology 2006;104:847–64. National Board of Echocardiography, http://www.echoboards. org/certification/certexpl.html (as of 1/10/2009). Block FE, Nuutinen L, Ballast B. Optimization of alarms: a study on alarm limits, alarm sounds and false alarms intended to reduce annoyance. J Clin Monit Comput 1999;15:75–83. IEC 60601-1-8 (2005–08): Medical electrical equipment – Part 1–8: General requirements for safety – Collateral standard: general requirements, tests and guidance for alarm systems in medical electrical equipment and medical electrical systems. Geneva: International Electrotechnical Commission, 2005. Imhoff M, Kuhls S. Alarm algorithms in critical care monitoring. Anesth Analg 2006;102:1525–37.

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Chapter

3

Validity, accuracy, and repeatability of monitoring variables Daniel M. Thys and Jung Kim

Introduction Most of the physiologic variables (they are variables, not parameters, because they vary from individual to individual) that we monitor in our daily practice are expressed as numerical values.1 There are many advantages to the conversion of physiologic activities into numbers. In the digital age, numbers are easy to compute, analyze, display, or convert into graphic format. Additionally, most of us are very comfortable with the use of numbers. From early ages, we are able to estimate numbers in a linear manner.2 We have an intrinsic understanding of what a “normal” value represents, of how a “range” characterizes the limits of a normal value, and how the magnitude of a change in a numerical value quantitates a deviation from normal physiologic function. We can intervene to correct abnormal values and tailor our response to the magnitude of the numerical change that we intend to achieve. The purpose of this chapter is to reflect on numbers as representations of physiologic data. Many different variables will be alluded to, but to make the analysis more palatable, one variable, cardiac output (CO), will frequently be used as an example. Cardiac output was selected because it constitutes an important physiologic variable that we are keen to monitor, because it has been studied extensively and because new techniques to monitor CO continue to be introduced. Under no circumstances should this chapter be construed as a detailed review of CO monitoring. Such a review is provided in Chapter 8.

What is the monitored variable? “My patient’s heart rate is 96 beats per minute.”

The definition of heart rate is self-explanatory and has been known to us since long before we entered medical school: heart rate is the number of heartbeats per unit of time, usually expressed as beats per minute (bpm). The principal purpose of heart rate monitoring is to detect numerical changes from normal or baseline. A low number draws our attention to various potential physiologic disturbances, whereas a high number suggests other disorders. We know that for the normal adult, the average heart rate is around 70 bpm. We are also well aware that it is more rapid in younger age groups. A heart rate of 96 bpm may be bradycardia in the newborn, but tachycardia in the elderly. In our practice, we interpret a numerical value such

16

as heart rate within the context of its clinical setting. As scientific knowledge expands, however, the context within which a numerical value needs to be interpreted broadens. Monitoring devices incorporate a variety of smoothing technologies to provide us with a relatively steady heart rate number that is free of artifacts. In our effort to obtain a steady or reliable heart rate number, however, we may be shrinking the clinical context and ignoring information that is of great value. When we observe changes in heart rate, they are usually the result of changes in the tone of the autonomic nervous system or reflex responses triggered by these changes. In a recent editorial, Deschamps and Denault explained how, in the future, the study of heart rate variability by quantitating autonomic tone may help us anticipate changes in heart rate and blood pressure.3 This knowledge would allow us to apply our therapeutic interventions with greater efficacy. To gauge heart rate variability, time intervals between cardiac contractions are measured, and their variability is analyzed using statistical analysis or other techniques. Absence of, or a decrease in, heart rate variability has been associated with various disease states, poor prognosis, and negative outcomes.4–9 On the contrary, preservation of, or increase in, heart rate variability has been related to good health and identified as a predictor of survival in critically ill patients.7,8 More recently, gender and postural position have been independently associated with heart rate (Figure 3.1).10 In the supine position, heart rate is higher in women than in men, whereas on standing, heart rate increases significantly in both genders. Additionally, investigators have observed that in middle-aged women, parasympathetic modulation dominates heart rate control, whereas sympathetic tone is dominant in middle-aged men (Figure 3.2).11 Finally, attention has recently turned to another measure of heart rate, called intrinsic heart rate (HRint ). HRint is defined as the heart rate seen in the absence of ongoing sympathetic or parasympathetic influences on the heart.12 We all know that heart rate increases with exercise, yet we also know that the maximal heart rate (HRmax ) that can be achieved during exercise decreases with age. Christou and colleagues have investigated the mechanisms that underlie these age-related differences.13 They observed that the lower mean HRmax achieved by older men is associated with lower mean levels of HRint and chronotropic responsiveness to ␤-adrenergic

Chapter 3 – Validity, Accuracy, and Repeatability of Monitoring Variables

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Figure 3.1. Influence of sex, generation, and posture on RR interval (Psex , Pgn , Ppos , respectively) and two-way interaction terms. RR interval is the inverse of heart rate. Reproduced with permission from reference 10.

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“My patient’s blood pressure is 137/81.”

We routinely refer to normal arterial pressure as being 120 over 80 mmHg. This is certainly correct when considering average blood pressures measured by cuff inflation in large adult populations. In individual patients, however, the normal blood pressure may vary significantly from these values, depending on the method of measurement. There is a large volume of literature documenting differences in blood pressure measurements depending on whether the variable was measured by sphygmomanometry, oscillometry, or invasive methods.14–17 Even within each technique, measurements will vary depending on equipment and procedures: aneroid versus mercury

Figure 3.2. Effect of gender and age on all measures of heart rate variability at five-year intervals from 40 to 79 years. (HF: high frequency; LF: low frequency; ln: natural logarithm; • male; ◦ female). Values are means ± SE; nu, no units (normalized). ∗ P ⬍ 0.05; P ⬍ 0.01 between genders by Student’s t-test. Modified and reproduced with permission from reference 11.

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stimulation when compared with young healthy men. They also noted that among individual subjects, HRint shows a particularly strong correlation with HRmax (Figure 3.3). The purpose of this brief discussion is not to review the autonomic determinants of heart rate, but to highlight the complexity of interpreting a single number, such as heart rate. A heart rate of 96 bpm can have widely differing meanings, depending on the clinical context. In a critically ill patient, a heart rate of 96 bpm will carry negative outcome implications if heart rate variability is absent. However, if heart rate variability is preserved, survival may be more likely. Similarly, a heart rate of 96 bpm may constitute one patient’s HRmax ; additional stress or ␤-adrenergic stimulation is unlikely to result in further increases in heart rate and/or CO. In a different subject, the

1.0

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same heart rate may be well below the HRmax ; it all depends on the patient’s HRint . As scientific knowledge evolves, it will become more and more challenging to provide a suitable context for each numerical value; our example of a heart rate of 96 bpm may need to be qualified for the patient’s age, gender, HRint , and heart rate variability, among many variables. It will be interesting to observe how monitoring technology evolves to incorporate some of these qualifiers into the monitoring of standard physiologic variables.

Psex × pos = 0.26 600

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Figure 3.3. Relation between maximal exercise heart rate and intrinsic heart rate. Modified and reproduced with permission from reference 13.

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Monitoring in Anesthesia and Perioperative Care

Reflected wave

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Figure 3.4. Carotid pressure waveform showing the forward and reflected wave pressures. Modified and reproduced with permission from reference 22.

manometer in sphygmomanometry, first-reading effect in oscillometry (the first of several readings obtained within a few minutes of each other tends to be higher, by about 3 to 5 mmHg, than subsequent readings), and location of the intraarterial catheter for invasive measurements.18,19

Because invasive blood pressure is often considered to be more reliable than noninvasive blood pressure, it is worth taking a closer look at its measurement. As the arterial pressure wave travels down the aortic tree, it is amplified by reflected waves and its amplitude increases in the periphery (Figures 3.4 and 3.5).20 The magnitude of the reflected wave will depend on a complex relationship among the patient’s age, the elastic properties of the arterial tree, and the location of the pressure measurement.21 Wave reflection is most pronounced in subjects between the ages of 20 and 40. In a 2004 study, Mitchell and associates have shown that in healthy middleaged and elderly individuals with no known cardiovascular disease, aortic stiffness increases dramatically with advancing age, whereas the stiffness of second- and third-generation muscular arteries increases minimally with age (Figure 3.6).22 Therefore, in healthy elderly subjects, changes in central aortic stiffness and forward wave amplitude, rather than wave reflection, are responsible for most of the increase in pulse pressure. These

ECG

Ao V

ASC Ao

HI D Ao MID T Ao 50 mm Hg DIAP Ao ABD Ao

TERM Ao

ECG

1 SECOND Figure 3.5. Pressure waveforms as a function of location from the ascending aorta to the iliac bifurcation in one patient. Figure constructed from single pulse or pairs of pulses selected from cardiac cycles with equal RR intervals and from similar phases of respiration. Ao V = sensor just above aortic valve; Asc Ao = ascending aorta; Hi D Ao = high descending aorta; Mid T Ao = midthoracic aorta; Diap Ao = diaphragmatic aorta; Abd Ao = abdominal aorta; Term Ao = terminal abdominal aorta just before iliac bifurcation. Reproduced with permission from reference 20.

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Chapter 3 – Validity, Accuracy, and Repeatability of Monitoring Variables

Figure 3.6. Means of regional pulse wave velocities (PWVs) and reflected wave variables by sex and decade of age. Carotid–femoral PWV increased substantially with advancing age (age2 term), whereas an insignificant increase in carotid–brachial PWV was found in these unadjusted analyses. As a result, carotid–femoral PWV exceeded carotid–brachial PWV in older participants. Aortic stiffening was accompanied by a proportional decrease in reflected wave transit time in younger but not older groups; therefore, distance to the effective reflecting site increased in older individuals. Numbers per group (men/women): ⬍50 years, n = 43/52; 50 to 59 years, n = 74/172; 60 to 69 years, n = 57/82; and 70+ years, n = 14/27. Reproduced with permission from reference 22.

observations provide insights into the variable mechanisms of age-related loss of peripheral pressure amplification: In young adults with a reflected pressure wave arriving centrally during diastole, pulse pressure is substantially higher in the periphery as compared with the central aorta. In middle age, increasing pulse wave velocity leads to premature return of the reflected pressure wave to the central aorta during systole, which augments central systolic and pulse pressure and reduces peripheral amplification. Finally, in the elderly, central arterial stiffness exceeds peripheral arterial stiffness. This loss of the normal arterial stiffness gradient reduces amplification and reflection. These changes are more pronounced in women than in men. In summary, invasive systolic and diastolic blood pressure recordings will vary with the sampling location (central versus peripheral), the age of the patient (young versus middleaged versus elderly), and the patient’s gender. Compared with central aortic pressure, invasive pulse pressure measured in the dorsalis pedis artery will be markedly amplified in the young, moderately amplified in the middle-aged, and equivalent in the elderly. Gender may further accentuate these differences. Normal blood pressure is indeed a complicated concept. In many instances, it will be difficult to interpret a blood pressure value

of 137/81 mmHg if the patient’s characteristics and the method of pressure measurement are unknown. Similar limitations are associated with the monitoring of most other variables. At first glance, the definition of CO is also straightforward: it is the volume of blood pumped in one minute by the heart. In the laboratory, CO can be measured accurately because the blood ejected by the heart in one minute can be collected and measured. In clinical practice, however, such a simple measurement is obviously not available; over the years, a variety of indirect measures of CO have been introduced. The earliest method was described by Adolph Fick in 1870 and was based on the principle that oxygen consumption is equal to the product of blood flow and oxygen consumed by the tissues.23 The calculation of CO by the Fick principle requires that in addition to oxygen consumption, the oxygen content of arterial and mixed venous blood be measured. Subsequently, different techniques, including indicator dilution, Doppler velocimetry, pulse pressure analysis, impedance cardiography, CO2 or inert gas rebreathing, and echocardiographic volumetry, have been introduced.24–27 In each of these techniques, different entities are being measured and different assumptions relied on to derive CO; each method also has its own limitations and intrinsic errors. The major limitations of the direct Fick technique are well recognized. They are related to errors in sampling and analysis, or to the inability to maintain steady-state hemodynamic and respiratory conditions. To minimize errors in sampling, the venous blood must be truly mixed venous blood and the samples must represent average, rather than instantaneous, samples. The most serious errors in the measurement of CO by the direct Fick technique result from changes in pulmonary volumes. Indeed, the methods used to measure oxygen consumption measure the uptake of oxygen by the lungs, rather than by the blood. Because lung volumes can change, the tissues’ oxygen consumption is not necessarily being measured. In addition to these technical exigencies, one must wonder about the clinical usefulness of a CO measurement technique that requires steady-state conditions; indeed, it is during conditions of hemodynamic instability that CO measurements are of the greatest use. Limitations of other CO measurement techniques are also manifold. In the dilution techniques, errors result from inadequate mixing and recirculation of the dye, as well as from respiratory variability. Doppler measurements are dependent on beam orientation and flow profile assumptions. Thoracic impedance measurements are influenced by lead placement and body habitus assumptions. In brief, none of these techniques is devoid of problems, and therefore establishing their accuracy is challenging.

How accurate is the measurement? “My patient’s cardiac output is 4.76 L/min.”

Accuracy is the degree of closeness of a measured or calculated variable to its true value. In the physical sciences, the

19

Monitoring in Anesthesia and Perioperative Care

20

4 Difference in CO (L/min) (COR – COT)

accuracy of a measurement technique is usually determined by repeatedly measuring a well-defined reference standard. The reference standards are obtained from an organization such as the National Institute of Standards and Technology. This federal organization supplies industry, academia, government, and other users with more than 1300 reference materials that are of the highest quality and have metrologic value. Obviously, there is no equivalent process to characterize the accuracy of clinical monitoring techniques. When the accuracy of a new CO technique is investigated, it often involves a comparison with thermodilution. But is thermodilution CO truly a valid standard? As mentioned previously, CO can be measured accurately if the heart’s output is pumped into a measurement bucket and quantitated over time. Although this approach is not practical in the clinical environment, it is certainly feasible in the laboratory. Interestingly, thermodilution has been studied in vitro, using a variety of mechanical models to produce precisely controlled blood flows.28–33 Although not all these studies are comparable, there is broad agreement that thermodilution measurements deviate from the calibrated flows by ± 10 percent to 20 percent. Therefore, the concept of thermodilution as a gold standard is mostly fallacious. As a similar absence of true quantity or absolute standards applies to many clinical variables, a different approach is necessary to validate the accuracy of new monitoring techniques. In their landmark publication, Bland and Altman addressed this issue.34 The statistical method that they described allows one to compare a new method with an established technique rather than with a true quantity. The purpose of such an analysis is to define by how much the new method is likely to differ from the old technique. If the new method differs little from the old method, the two techniques can be used interchangeably. Ideally, the clinically acceptable difference will be defined before conducting the comparison; this facilitates interpretation of the results and the selection of a sample size. In a comparison of two measurement techniques, a first step consists of building a plot with the difference between the results obtained with each of the two methods on the vertical axis and the mean of the results on the horizontal axis (Figure 3.7). One must then establish that there is no pattern or relationship in the plot of the averages versus the differences; it may be useful to calculate a correlation coefficient for the data and test it against the null hypothesis of r = 0. Assuming that there is no obvious relationship between the differences and the mean, one can calculate the bias and the limits of agreement. The bias is equal to the mean of the differences, whereas the 95 percent limits of agreement are the bias plus and minus two standard deviations of the differences (this assumes a normal or Gaussian distribution of the differences). If the bias or mean difference is small, it can be ignored. If the bias is consistent, an adjustment can be applied; one can subtract the bias or mean difference from the new method. The 95 percent limits of agreement are used to determine the clinical validity of the new technique. As stated earlier, ideally the acceptable

+ 2 Standard deviations

2 Bias

0

-2

– 2 Standard deviations

-4 0

2 4 6 Mean cardiac output (L/min) (COR + COT)/2

8

Figure 3.7. Typical Bland–Altman plot for the comparison of two cardiac output techniques (COR : cardiac output from reference technique; COT : cardiac output from tested technique).

difference between the two techniques would have been defined before the conduct of the comparison. If the differences within the 95 percent limits of agreement are not clinically important, the two measurements methods can be used interchangeably. Bias analysis has been used extensively in the evaluation of new CO monitoring techniques and examples from the literature will be used to clarify this method of comparison. To assess the validity of a new continuous CO (CCO) device, Bein and associates studied 113 CO measurements in 10 patients and compared them with measurements of CO by pulse contour analysis and ultrasound (Doppler) techniques.35 The authors plotted the mean of the results on the horizontal axis and the difference between the results on the vertical axis. As indicated previously, the next step in the analysis consists of determining whether an obvious relationship exists between the differences and the mean results. For both comparisons, this certainly was the case (r = – 0.69 and r = – 0.52, respectively; Figures 3.8 and 3.9). When compared with pulse contour and ultrasound, the new technique (CCO) appeared to systematically overestimate CO at low values (2 to 4 L/min) and to underestimate CO at high values (⬎ 5 L/min). When such a data distribution occurs, little useful information can be derived from the bias calculation (Bland and Altman suggest that a log transformation of the data may occasionally be helpful). Indeed, the purpose of the bias calculation is to define the systematic adjustment that needs to be made to the measurements by the new technique so they are in agreement with those of the established technique. In the current example, one would need to make a negative adjustment at low CO, no adjustment at normal CO, and a positive adjustment at high CO. Clinically, this is highly impractical. In a different study, Missant et al. compared CO by pulse contour analysis and Doppler echocardiography with thermodilution CO.36 The investigators compared 149 pulse contour measurements with 84 Doppler measurements with thermodilution in 20 patients. When the means of the results were plotted on the horizontal axis and the difference between the results

Chapter 3 – Validity, Accuracy, and Repeatability of Monitoring Variables

Figure 3.8. Bland–Altman plot between continuous cardiac output (CCO) and pulse-contour cardiac output (PCCO) techniques. The solid line represents the mean difference (bias); the dotted line represents the 2SD limits of agreement. Dotted circles added for emphasis. Modified and reproduced with permission from reference 35.

2.00

Diff (CCO – PCCO)

1.00

0.00

–1.00

–2.00

–3.00

–4.00 2.00

2.50

3.00

3.50

4.00

4.50

5.00

5.50

6.00

6.50

7.00

Mean (CCO + PCCO)

on the vertical axis, no obvious relationship could be discerned for either comparison (Figures 3.10 and 3.11). For a range of CO values between 2 and 7.5 L/min, the data points distributed randomly around the average difference between the measurements. The bias or average difference between the measurements was –0.03 L/min for the comparison between pulse contour and thermodilution, and +0.45 L/min for the comparison between Doppler and thermodilution. Although a systematic error of –0.03 L/min has little clinical significance and can be ignored, the same most likely cannot be said about an error of 0.45 L/min. Therefore, CO measured by the Doppler technique

that is described in the manuscript would require a systematic adjustment of +0.45 L/min to be comparable with thermodilution CO. The next step in the analysis of the results requires that the 95 percent limits of agreement be calculated (± 2 standard deviations of the differences). For the comparison between pulse contour and thermodilution, they were found to be +1.26 L/min and –1.33 L/min, whereas they were +2.38 L/min and –1.49 L/min for Doppler and thermodilution. Finally, one must decide whether the 95 percent limits of agreement are clinically acceptable. In the current example, assuming a true CO of

3.00

Diff (CCO – UCCO)

2.00 1.00 0.00 –1.00 –2.00 –3.00 –4.00 2.00

3.00

4.00

5.00

6.00

7.00

Mean (CCO + UCCO) Figure 3.9. Bland–Altman plot between continuous cardiac output (CCO) and ultrasound cardiac output (UCCO) techniques. The solid line represents the mean difference (bias); the dotted line represents the 2SD limits of agreement. Dotted circles added for emphasis. Modified and reproduced with permission from reference 35.

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Figure 3.10. Bland–Altman plot of cardiac output measurements by pulmonary artery thermodilution (COTD ) and pulse contour analysis (COPC ). Reproduced with permission from reference 36.

4 3 2 (L/min)

Difference COTD and COPC

Monitoring in Anesthesia and Perioperative Care

1 0 –1 –2 Bias –0.03 2SD 1.30

–3 –4 0

1

2

3 4 5 Average COTD and COPC (L/min)

6

One must obviously keep in mind that these findings apply only to this one specific study. Indeed, other studies yield very different findings. When Darmon and colleagues compared CO by Doppler echocardiography and thermodilution, they found a percentage error of 19 percent.38 Such an error is well within the acceptable range and, in these latter investigators’ clinical practice, Doppler echocardiography and thermodilution are interchangeable. The reasons that studies can yield such divergent findings are myriad and related to differences in patient population, experimental circumstances, and methodological variations. Evidently, a clinician can draw conclusions about the acceptability of a new technique only by consulting the broadest body of evidence available. Although Bland–Altman analysis is now widely used in the assessment of new monitoring techniques, clinically acceptable 95 percent limits of agreement are seldom defined before the onset of a study. In a review by Mantha and associates of 42 anesthesia reports that used limits of agreement methodology to analyze comparisons between measurement techniques, only three reports included an a priori definition of limits of agreement.39 Furthermore, the 30 percent acceptability criteria that were defined by Critchley and Critchley for the comparison of new CO techniques with thermodilution cannot be applied to the comparison of measurement techniques for other variables, as they sometimes are.40 Clearly, for each physiologic variable,

Figure 3.11. Bland–Altman plot of cardiac output measurements by pulmonary artery thermodilution (COTD ) and pulse contour analysis (COecho ). Reproduced with permission from reference 36.

3 2 1 0 –1 –2 Bias 0.45 2SD 1.93

–3 –4 0

22

8

4

(L/min)

Difference COTD and COecho

4.5 L/min, pulse contour analysis will yield CO values between 3.2 L/min and 5.8 L/min in 95 percent of measurements. For Doppler echocardiography, they will fall between 2.57 L/min and 6.43 L/min. Are those values clinically acceptable? In 1999, Critchley and Critchley published a very elegant study that answered this question.37 They conducted a metaanalysis of studies that compared methods of CO measurement and used Bland–Altman statistics for analysis. They identified 25 comparative studies and stated that acceptance of a new method of CO measurement needed to be judged against the accuracy of the reference method. In most studies, the reference method is thermodilution, which has an accuracy of ± 20 percent, as stated earlier. They concluded that a new CO measurement technique should be accepted if the percentage error (± 2 standard deviations divided by the mean CO for the study) did not exceed ± 30 percent. We can now apply these acceptability criteria to the study of Missant et al. Although the authors do not provide the mean CO for the study, one can deduce from the published data that it was 4.5 L/min. Therefore, the percentage error for pulse contour analysis was 29 percent (2 standard deviations = 1.3; mean CO = 4.5 L/min; percentage error = 1.3/4.5). This falls within the acceptable range as defined by Critchley and Critchley, and thus pulse contour analysis can be substituted for thermodilution. For Doppler echocardiography, the percentage error was 43 percent and thus, in these investigators’ experience, it is not an acceptable substitute for thermodilution.

7

1

2

3 4 5 6 Average COTD and COecho (L/min)

7

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Chapter 3 – Validity, Accuracy, and Repeatability of Monitoring Variables

clinically acceptable limits need to be determined. For example, in a study of transcutaneous PCO2 monitoring devices, the clinically acceptable limits were set at ± 7.5 mmHg.41 How such a value was arrived at is unclear, but it is at least a step in the right direction. The European Society of Hypertension recommends that automated sphygmomanometers differ from a mercury standard by a standard deviation of less than 8 mmHg.42,43 For laboratory analysis of PO2 and PCO2 , limits of ± 7.5 percent have been recommended.44

How reproducible is the measurement? “My patient’s second cardiac output is 4.15 L/min.”

When interpreting data from a monitoring or measurement technique, it is important to know not only the technique’s accuracy, but also its repeatability or reproducibility. Indeed, from a clinical standpoint, one needs to know whether the second measurement of a variable is significantly different from a prior measurement. Does the new value represent a true decrease in CO (e.g., a real decrease of 13% from 4.76 L/min to 4.15 L/min), or are the two values within the measurement technique’s expected range of variability? To understand the difference between accuracy and reproducibility, it is useful to refer to a target comparison (Figure 3.12). If a number of rounds are fired at a target, accuracy will describe the closeness of the hits to the bull’s-eye of the target. Rounds that hit close to the center of the target are considered to be accurate. As additional rounds are fired, their location in relation to prior hits will determine reproducibility. If all the hits are clustered together, the reproducibility is

considered to be high (Figure 3.12A, C); if they are widely dispersed, the reproducibility is low (Figure 3.12D). A few additional observations are worth considering. (1) As shown in Figure 3.12C, a measurement system can have high reproducibility, but low accuracy. The reverse is not true, however. For a system to be accurate, the hits must be close to the center of the target, and therefore, by necessity, they will also be close together. (2) Average accuracy measurements can be misleading. Indeed. if one were somehow able to calculate an average accuracy for the four hits in Figure 3.12D, one would end up with a high mean accuracy (a hit above the center is counterbalanced by a hit below the center, etc.). However, each individual hit is highly inaccurate and poorly reproducible. Therefore, knowing a measurement system’s average accuracy without knowing its reproducibility is of limited use. When Bland and Altman published their method to test agreement between two methods of clinical measurement, they also referred to repeatability as relevant to the assessment of agreement. It is indeed obvious that if there is considerable variability in the results obtained with a certain method, agreement with another method will, by definition, be poor. To gauge reproducibility, they suggest that a coefficient of repeatability be calculated. This can be done in a manner similar to the one used to test the limits of agreement: the mean of repeated measurements are plotted on the horizontal axis, and the differences between measurements are plotted on the vertical axis. Theoretically, the mean of the differences should be zero, as the same measurement method was used. The standard deviation of the differences is calculated, and the value of two standard deviations is considered to be the coefficient of repeatability. The coefficient of repeatability represents the value below which the Figure 3.12. Target comparison of accuracy and reproducibility. (A) High accuracy and reproducibility; (B) moderate accuracy and reproducibility; (C) low accuracy and high reproducibility; (D) low accuracy and reproducibility.

A

B

C

D

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Monitoring in Anesthesia and Perioperative Care

absolute difference between two repeated test results is expected to lie, with a probability of 95 percent. If several repeated measurements are obtained per subject, the standard deviations of the measurements are plotted against their mean and analyzed by one-way analysis of variance. It is worth noting that when Mantha and colleagues analyzed the anesthesia literature, they observed that repeatability was assessed in only 9 of 42 reports (21.4%). In addition, the manner by which repeatability was evaluated varied markedly from study to study. For instance, Seguin and associates used two different approaches to assess reproducibility of semicontinuous thermodilution CO and bolus thermodilution CO.45 The first approach was the one described by Stetz and colleagues in 1982.46 The Stetz group reviewed 14 publications on the use of thermodilution in clinical practice and concluded that with the use of commercial thermodilution devices, a minimal difference of 12 percent to 15 percent (average 13%) between determinations was required to be statistically significant, provided that each determination was obtained by averaging three measurements. If each determination was the result of only a single measurement, a minimal difference of 20 percent to 26 percent (average 22%) was required for statistical significance. In practice, a standard error of the mean can be calculated for the measurements. A variation of at least three standard errors of the mean is necessary to establish with confidence that two values of CO differ from each other. With this analysis, Seguin and associates determined that the threshold required to establish that two CO measurements are different was 0.54 L/min for bolus CO and 0.465 L/min for continuous CO. Although they also tested repeatability by the Bland–Altman method, they did not provide a coefficient of repeatability for their measurements, and therefore, the meaning of their analysis is unclear. Reproducibility will be influenced by myriad factors, some intrinsic to the measurement technique and others determined by technical aspects of the measurement. These technical factors have been well studied for thermodilution CO. Factors such as temperature and volume of injectate, speed and rate of injection, and timing in the respiratory cycle have all been shown to influence the reproducibility of thermodilution CO.47,48 Finally, two additional observations related to this discussion of accuracy and reproducibility merit comment. First, in most of the studies that were referenced previously, the number of data points plotted in the Bland–Altman analysis exceeds the number of studied patients – that is, multiple measurements are included for each patient. Therefore, the bias analysis will be influenced not only by the differences between the two measurement techniques but also by the reproducibility of each of the measurement techniques. In most publications, however, this obvious limitation is never mentioned. Second, it is often suggested that the monitoring of changes in physiologic variables is more important than a focus on specific values. Even though this may be true, interpretation of change is feasible only if the repeatability of the measurement technique is known. As mentioned earlier, most investigations of new measurement techniques fail to include an analysis of

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reproducibility. In its absence, the meaning of changes cannot be interpreted.

Conclusions In our daily management of patients, we collect a large quantity of numbers from a variety of physiologic monitors. We interpret these values and tailor our therapeutic interventions to the results of our interpretations. The purpose of this brief discussion was to stimulate thought about the meaning of some of the numbers that we use in our clinical management. The following conclusions can be drawn: 1. An individual value, even one as simple as heart rate, is meaningless if it is not analyzed within its clinical context; as scientific knowledge expands, the importance of the clinical context increases. 2. For each measured variable, the values that one obtains will be influenced by a large number of factors. These include the underlying physiologic process, but also factors related to patient characteristics, the measurement technique, and the manner in which the technique is applied. 3. It is seldom possible to determine the accuracy of a new measurement technique, because reference standards rarely exist in clinical medicine. The best one can hope for is to ascertain whether a new technique is interchangeable with an older, established technique. The Bland–Altman analysis was designed to test such interchangeability. 4. One needs to know the reproducibility of a measurement technique to gauge its value; a technique that yields results that are poorly reproducible is of limited value. In addition, because absolute values are often influenced by a large number of confounding factors, the monitoring of changes is often recommended. However, changes cannot be interpreted if one does not know the measurement technique’s reproducibility.

References 1. Altman DG, Bland JM. Variables and parameters. Br Med J 1999; 318:1667. 2. Ebersbach M, Luwel K, Frick A, Onghena P, Verschaffel L. The relationship between the shape of the mental number line and familiarity with numbers in 5- to 9-year old children: Evidence for a segmented linear model. J Exper Child Psychol 2008;99:1–17. 3. Deschamps A, Denault A. Analysis of heart rate variability: a useful tool to evaluate autonomic tone in the anesthetized patient? Can J Anaesth 2008; 55(4):208–13. 4. Carpeggiani C, Emdin M, Raciti M, et al. Heart rate variability and myocardial infarction: acute and sub-acute phase. CNR-PF FATMA Multicenter Study on psycho-neurological risk factors in acute myocardial infarction. Clin Sci (Lond) 1996;91 Suppl:28–9. 5. Piepoli M, Coats AJ. Autonomic abnormality in chronic heart failure evaluated by heart rate variability. Clin Sci (Lond) 1996;91Suppl:84–6.

Chapter 3 – Validity, Accuracy, and Repeatability of Monitoring Variables

6. Voss A, Wessel N, Sander A, Malberg H, Dietz R. Requirements on sampling rate in Holter systems for analysis of heart rate variability. Clin Sci (Lond) 1996;91 Suppl:120–1. 7. Maier P, Toepfer M, Dambacher M, Theisen K, Roskamm H, Frey AW. Heart rate variability and its relation to ventricular tachycardia in patients with coronary artery disease. Clin Sci (Lond) 1996;91Suppl:67. 8. Schmidt H, Muller-Werdan U, Hoffmann T, et al. Autonomic dysfunction predicts mortality in patients with multiple organ dysfunction syndrome of different age groups. Crit Care Med 2005;33:1994–2002. 9. Winchell RJ, Hoyt DB. Analysis of heart-rate variability: a noninvasive predictor of death and poor outcome in patients with severe head injury. J Trauma 1997;43:927–33. 10. Stolarz K, Staessen J, Kuznetsova T, et al. Host and environmental determinants of heart rate and heart rate variability in four European populations. J Hypertens 2003;21:525–35. 11. Kuo TBJ, Lin T, Yang CCH, Li CL, Chen CF, Chou P. Effect of aging on gender differences in neural control of heart rate. Am J Physiol Heart Circ Physiol 1999;277:H2233-H2239. 12. Joyner MJ. Not so fast: intrinsic heart rate vs. beta-adrenergic responsiveness in the aging human heart. J Appl Physiol 2008;105(1):3–4. 13. Christou D, Seals D. Decreased maximal heart rate with aging is related to reduced ␤-adrenergic responsiveness but is largely explained by a reduction in intrinsic heart rate. J Appl Physiol 2008;105(1):24–9. 14. Park MK, Menard SW, Yuan C. Comparison of auscultatory and oscillometric blood pressures. Arch Pediatr Adolesc Med 2001;155:50–53. 15. Goonasekera CD, Dillon MJ. Random zero sphygmomanometer versus automatic oscillometric blood pressure monitor; is either the instrument of choice? J Hum Hypertens 1995;9:885–9. 16. Gillman MW, Cook NR. Blood pressure measurement in childhood epidemiological studies. Circulation 1995;92: 1049–57. 17. Park MK, Menard SM. Accuracy of blood pressure measurement by the Dinamap monitor in infants and children. Pediatrics 1986;79:907–14. 18. Perloff D, Grim C, Flack J, et al. Human blood pressure determination by sphygmomanometry. Circulation 1993;88:2460–70. 19. Park MK, Menard SM. Normative oscillometric blood pressure values in the first 5 years in an office setting. Am J Dis Child 1989;143:860–4. 20. Murgo JP, Westerhof N, Giolma JP, Altobelli SA. Aortic input impedance in normal man: relationship to pressure wave forms. Circulation 1980;62:105–16. 21. Westerhof BE, Guelen I, Westerhof N, Karemaker JM, Avolio A. Quantification of wave reflection in the human aorta from pressure alone: a proof of principle. Hypertension 2006;48:595–601. 22. Mitchell GF, Parise H, Benjamin EJ, et al. Changes in arterial stiffness and wave reflection with advancing age in healthy men and women: the Framingham Heart Study. Hypertension 2004;43:1239–45. ¨ 23. Fick A. Uber die Messung des Blutquantums in den Hertzventrikln. Sitz Physik Med W¨urzburg 1870; p. 16. 24. Albert NM, Hail MD, Li J, Young JB. Equivalence of the bioimpedance and thermodilution methods in measuring cardiac output in hospitalized patients with advanced, decompensated chronic heart failure. Am J Crit Care 2004;13(6):469–79.

25. Haryadi DG, Orr JA, Kuck K, McJames S, Westenskow DR. Partial CO2 rebreathing indirect Fick technique for non-invasive measurement of cardiac output. J Clin Monit Comput 2000;16(5–6):361–74. 26. Spiess BD, Patel MA, Soltow LO, Wright IH. Comparison of bioimpedance versus thermodilution cardiac output during cardiac surgery: evaluation of a second-generation bioimpedance device. J Cardiothorac Vasc Anesth 2001;15(5): 567–73. 27. Parra V, Fita G, Rovira I, Matute P, Gomar C, Par´e C. Transoesophageal echocardiography accurately detects cardiac output variation: a prospective comparison with thermodilution in cardiac surgery. Eur J Anaesthesiol 2008;25(2):135–43. 28. Jebson P, Karkow W. Pulsatile flow simulator for comparison of cardiac output measurements by electromagnetic flow meter and thermodilution. J Clin Monit 1986;2:6–14. 29. Bilfinger TV, Lin CY, Anagnostopoulos CE. In vitro determination of accuracy of cardiac output measurements by thermal dilution. J Surg Res 1982;33(5):409–14. 30. Norris SL, King EG, Grace M, Weir B. Thermodilution cardiac output – an in vitro model of low flow states. Crit Care Med 1986;14(1): 57–9. 31. Runciman WB, Ilsley AH, Roberts JG. An evaluation of thermodilution cardiac output measurement using the Swan-Ganz catheter. Anaesth Intensive Care 1981;9(3): 208–20. 32. Powner DJ, Snyder JV. In vitro comparison of six commercially available thermodilution cardiac output systems. Med Instrum 1978;12(2):122–7. 33. Renner LE, Morton MJ, Sakuma GY. Indicator amount, temperature, and intrinsic cardiac output affect thermodilution cardiac output accuracy and reproducibility. Crit Care Med 1993;21(4):586–97. 34. Bland JM, Altman DG. Statistical methods for assessing between two methods of clinical measurement. Lancet 1986; 1(8476):307–10. 35. Bein B, Worthmann F, Tonner PH, Paris A, Steinfath M, Hedderich J, Scholz J. Comparison of esophageal Doppler, pulse contour analysis, and real-time pulmonary artery thermodilution for the continuous measurement of cardiac output. J Cardiothorac Vasc Anesth 2004;18:185–189. 36. Missant C, Rex S, Wouters, PF. Accuracy of cardiac output measurements with pulse contour analysis (PulseCO) and Doppler echocardiography during off-pump coronary artery bypass grafting. Eur J Anaesthesiol 2008;25:243–48. 37. Critchley LAH, Critchley JAHJ. A meta-analysis of studies using bias and precision statistics to compare cardiac output measurement techniques. J Clin Monit Comput 1999;15: 85–91. 38. Darmon PL, Hillel Z, Mogtader A, Mindich B, Thys D. Cardiac output by transesophageal echocardiography using continuous-wave Doppler across the aortic valve. Anesthesiology 1994;80(4):796–805. 39. Mantha S, Roizen MF, Fleisher LA, Thisted R, Foss J. Comparing methods of clinical measurement: reporting standards for Bland and Altman analysis. Anesth Analg 2000;90(3):593–602. 40. Molnar Z, Umgelter A, Toth I, et al. Continuous monitoring of ScvO(2) by a new fibre-optic technology compared with blood gas oximetry in critically ill patients: a multicentre study. Intensive Care Med 2007;33(10):1767–70. 41. Bendjelid K, Sch¨utz N, Stotz M, Gerard I, Suter PM, Romand JA. Transcutaneous PCO2 monitoring in critically ill adults: clinical

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evaluation of a new sensor. Crit Care Med 2005;33(10): 2203–6. 42. Association for the Advancement of Medical Instrumentation. American National Standard. Electronic or Automated Sphygmomanometers. ANSI/AAMI SP 10–1992. Arlington, VA: AAMI, 1993:40. 43. O’Brien E, Waeber B, Parati G, Staessen J, Myers MG. Blood pressure measuring devices: recommendations of the European Society of Hypertension. BMJ 2001;322:531–6. 44. Zollinger A, Spahn DR, Singer T, et al. Accuracy and clinical performance of a continuous intra-arterial blood-gas monitoring system during thoracoscopic surgery. Br J Anaesth 1997;79: 47–52.

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45. Seguin P, Colcanap O, Le Rouzo A, Tanguy M, Guillou YM, Malledant Y. Evaluation of a new semi-continuous cardiac output system in the intensive care unit. Can J Anesth 1998;45:578–83. 46. Stetz CW, Miller RG, Kelly GE, Raffin TA. Reliability of the thermodilution method in the determination of cardiac output in clinical practice. Am Rev Respir Dis 1982;126(6):1001–4. 47. Stevens JH, Raffin TA, Mihm FG, Rosenthal MH, Stetz CW. Thermodilution cardiac output measurement. Effects of the respiratory cycle on its reproducibility. JAMA 1985;253(15):2240–2. 48. Pearl RG, Rosenthal MH, Nielson L, Ashton JP, Brown BW Jr. Effect of injectate volume and temperature on thermodilution cardiac output determination. Anesthesiology 1986;64(6):798–801.

Chapter

4

Teaching monitoring skills Samuel DeMaria Jr., Adam I. Levine, and Yasuharu Okuda

Introduction Most medical schools and residency programs do not have a formalized training and assessment program dedicated to the acquisition of skills and knowledge needed for monitoring the perioperative patient. This is understandable, as the current model of medical education was developed during the early 20th century, when the act of monitoring during a procedure meant a very different enterprise from the current state of the art in anesthesiology. Typically, information related to monitor output was first learned piecemeal throughout medical school, and only when it was necessary to demonstrate changes in patient physiology related to a drug or disease process. It was rarely taught as a stand-alone topic, even at the graduate medical education (GME) level. Although the Accreditation Council for Graduate Medical Education (ACGME) defines the scope of practice for anesthesiology to include “monitoring and maintenance of normal physiology during the perioperative period” and mandates that anesthesiology residents have “significant experience with central vein and pulmonary artery catheter placement and the use of transesophageal echocardiography and evoked potentials,” a standardized curriculum and a standardized assessment for monitor training do not currently exist.1 Physicians in training learn monitoring skills in the same way they learn other procedures, by “seeing, doing, and teaching.” Over the past 20 years, there have been significant advances in available monitoring modalities. Although the complexity of monitoring has become daunting, physicians are now able to continuously measure physiologic parameters such as core temperature, end-tidal CO2 , and arterial blood pressure. With each of these advanced capabilities comes a need to learn new skills and knowledge in new ways. As an emphasis on patient safety and error reduction has become paramount, it is increasingly difficult for medical students and residents to “learn on the job” on actual patients. This situation creates an opportunity for innovative educators to develop and implement unique educational modalities using state-of-the-art technologies to teach and evaluate perioperative physiologic monitoring skills. The traditional method of passive learning through lectures and reading is not ideal for teaching the majority of monitoring skills, given the dynamic nature of these devices and the

data they generate. Although some basic concepts can be effectively taught in a lecture format, the development of psychomotor skills needed for invasive monitor placement, as well as the development of cognitive skills needed for data analysis, data synthesis, and data fidelity determination, are best been taught at the bedside. Unfortunately, the bedside teaching of monitoring skills has become challenging in the current medicolegal climate and has put an increased demand on faculty efficiency and productivity. Unlike passive instruction, adult learning theory emphasizes the need for adults to learn in an environment that promotes experience and self-direction.2 Based on this learning theory, adult learners need to understand the benefits of knowledge as well as its potential applications for their learning to be successful. This was corroborated by a review by Davis and associates.3 In an attempt to determine formal continuing medical education (CME) effectiveness, the authors reviewed a wide variety of CME formats, including conferences, refresher courses, seminars, lectures, and workshops, and explored the effect of formal CME on American, Canadian, and French internists, pediatricians, and family practitioners. The authors concluded that “interactive educational sessions that enhance participant activity and provide the opportunity to practice skills can effect change in professional practice and, on occasion, health care outcome.” They also concluded that “didactic sessions alone do not appear to be effective in changing physician performance.” Not surprisingly, increased learner participation and interaction between educator and student also increased overall satisfaction with the teaching program.4 Cantillion and Jones determined that although interactive experience is important, it is much more effective for the adult learner when it is accompanied by feedback.5 The use of evaluation and feedback was support by Reiter and associates, who determined that adults are not innately self-directed learners who can accurately assess their own strengths and weaknesses.6 It follows that educational modalities that encourage interactive, hands-on, small-group sessions that include immediate feedback would be the most effective. With the understanding of adult learning and effective teaching modalities, an innovative model for teaching monitoring skills that takes a logical, chronologic approach is described

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in this chapter. Implementing new technologies, such as simulation for monitor skill teaching, is also expanded on. Implementing such a program will afford the educator the opportunity to teach monitoring skills in an active and explicit fashion that is more likely to affect a student’s knowledge base in an efficient and effective way.

Philosophical framework for teaching monitoring skills in perioperative medicine The numerous effects of anesthesia on the normal physiologic state mandate that practitioners engaged in the delivery of perioperative care be facile with a number of monitoring skills and modalities. Only through such competence can the mission of the Anesthesia Patient Safety Foundation (APSF), “[t]hat no patient shall be harmed by anesthesia,” be realized. Successfully teaching such complex skills to clinicians and students relies on multimodality techniques based firmly in adult learning theory. Because the practitioner is the final common conduit through which all input gleaned from monitors passes, he or she should be optimally trained to process, interpret, and act on such information on the patient’s behalf. He or she must also understand that monitoring is a process that is ongoing and does not occur in isolation from other clinical information. Interpreting and placing physiologic monitors is second nature for the seasoned anesthesiologist. Many do not normally consider all the components involved with successfully monitoring patients in their day-to-day activities. Therefore, deconstructing the skills necessary for safe and effective patient monitoring placement and interpretation is critical in the development of an effective and systematic educational methodology of teaching monitoring skills. Monitoring skills can be divided into psychomotor and cognitive skills. These skills can be further subdivided into various components. Educators can determine from these lists which specific goals and objectives they hope to accomplish during a particular monitoring skills teaching session (Box 4.1). In 1999, the ACGME and the American Board of Medical Specialties (ABMS) defined competency in terms of six domains to be used in the evaluation of new practitioners (Table 4.1).7 In each of these domains, a set of unique knowledge, skills, and attitudes (which include behaviors) must be developed for the competencies to be achieved effectively. An effective way for educators to approach the teaching of monitoring skills is to consider the ACGME core competencies within a chronological framework to identify the attitudes, skills, and knowledge necessary at each step in the monitoring process in the preoperative, intraoperative, and postoperative periods. We have coined this framework the “ASK [attitudes, skills, and knowledge] to achieve” model for developing monitoring skills (Boxes 4.2, 4.3, and 4.4).

Preoperative phase Monitor selection and the timing of the monitor placement are critical components of monitoring skills. This preplacement

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Box 4.1 Psychomotor and cognitive components of monitoring skills Psychomotor skills Landmark identification Patient positioning Sterile patient and monitor kit preparation Development of an ergonomic work environment Hand–eye coordination Procedure sequence Intraprocedure troubleshooting Proper placement confirmation Securing monitor site Cognitive skills Monitor selection Indications Contraindications Monitor site insertion Indications Contraindications Timing of placement Preanesthetic induction Postanesthetic induction Monitor interpretation Data validity Data corroboration Data analysis Clinical management Development of differential diagnosis Therapeutic intervention Patient reassessment Monitor selection

stage is crucial to the anesthesia provider and is best approached systematically during the assessment of the patient and the anticipated surgical factors. Educators should emphasize which

Table 4.1.

The ACGME core competencies

Domain of competency Patient care Medical knowledge Practice-based learning and improvement Interpersonal and communication skills Professionalism Systems-based practice

Description of domain Compassionate and medically appropriate treatment of health problems Understanding of established and evolving medical evidence and the application of such evidence to patient care Evaluation of one’s own patient care and utilization of medical knowledge to improve the delivery of this care to patients Professional and appropriate interactions with patients and other health care providers to improve patient care Carrying out professional responsibilities, adherence to ethical tenets, and sensitivity to diversity Appropriate practice within the modern system of health care and the ability to effectively call on system resources to provide optimal care

Adapted from http://www.acgme.org/outcome/comp/compMin.asp.

Chapter 4 – Teaching Monitoring Skills

Box 4.2 Preoperative ASK to achieve 1. Evaluation of monitor necessity – Gather surgical/patient information that supports/obviates the need for the monitor – Consider indications/contraindications – Consider invasive versus noninvasive monitors – Consider the timing of invasive monitor placement – Consider the evidence and cost/benefit ratio (e.g., use of bispectral index monitor for a patient with a low preoperative risk of intraoperative awareness) – Discuss the decision to place or forgo the monitor with the surgical team and patient – Ensure that the patient understands risks/benefits and has had questions answered 2. Placement of monitors – – – –

Anticipate the logistics/ergonomics of monitor placement and use Master and practice the psychomotor skills necessary to safely place and activate monitor Ensure patient comfort Ensure patient safety (e.g., ultrasound-guided central venous catheter placement and maintenance of sterile technique)

–

–

Develop and adopt methods to combat error fixation and decreased vigilance (e.g., mandatory breaks and enabling all audible alarms) Develop and implement scanning skills

3 Intervention – – – – – –

Apply knowledge of normal values and predetermined thresholds to clinical scenario Decide what treatment is appropriate to correct a perceived abnormal monitor value Cross-check and double-check fidelity of data before intervening or failing to intervene Consider all corroborating and conflicting data Recognize that no intervention is without risks and benefits Communicate to appropriate team members that an intervention is being made

4 Reevaluation – – – –

Repeat steps 1–3 above after intervention as necessary Consider expected response to the intervention Communicate problems to team and seek assistance where appropriate Be a patient advocate despite potential conflicting pressures

Box 4.3 Intraoperative ASK to achieve

Box 4.4 Postoperative ASK to achieve

1 Interpretation of monitors – Consider the technology and theory behind the monitor of interest – Consider the strengths/weaknesses – Consider the importance of corroborating/conflicting data as well as interfering factors (e.g., effect of electrocautery on ECG tracing) – Consider common pitfalls (e.g., importance of a good waveform in interpretation of the pulse oximeter reading) – Understand and anticipate the normal values for the particular patient – Master the intricacies of reading monitor changes (e.g., recognition of cannon waves on the arterial line tracing in a patient with AV block) – Develop troubleshooting and salvage skills (e.g., fixing a positional monitor) – Determine threshold values at which to consider an intervention (e.g., decision to switch to 100% oxygen if pulse oximeter continues to read less than 92%) – Develop confidence in physical exam skills to confirm or disprove potentially erroneous data (i.e., appreciate the importance of the practitioner as a monitor) 2 Vigilance

1 Evaluation of monitor necessity – Use a similar approach to monitor necessity as in preoperative phase – Determine need for new monitors – Consider logistics/ergonomics of the postoperative setting (e.g., will the intensive care unit be able to use monitors already in place?) – Communicate effectively the monitoring endpoints used to intervene for the patient intraoperatively and any problems encountered with the monitors

–

Recognize and correct barriers to proper vigilance (e.g., fatigue and distraction)

2 Removal of monitors – –

Predetermine what defines “stable” and discontinue monitors that are no longer necessary Discontinue invasive monitors as soon as possible to prevent patient discomfort and likelihood of infection

monitors are standard (as defined by the ASA) and which monitor options are indicated and necessary based on the patient’s comorbidities and/or the anticipated surgical derangements. After the array of monitors to be used is determined, the timing of monitor placement must also be considered and taught. Should the monitor be placed before the anesthetic induction, or can the monitor be placed safely after the anesthetic induction? Are the indications for a particular monitor based on the patient’s comorbidities (e.g., severe coronary artery disease,

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raised intracranial pressure, decompensated congestive heart failure) or are the indications based on the anticipated surgical physiologic derangements? Will the data provided by the specific monitor be necessary for the administration of a safe anesthetic induction, or will these data be necessary only intraoperatively? The student or resident physician is obligated to conduct a thorough history, physical exam, and review of available medical records to determine what, if any, patient factors mandate monitoring beyond the ASA standards. In addition, the planned surgical technique, which often is an unknown variable to the novice anesthesia provider, should be discussed with more experienced anesthesia or surgical staff. This helps the novice anticipate important determinants of monitor choice (e.g., expected blood loss) and augments his or her knowledge of accepted indications for the monitor to be placed. This also offers an opportunity for communication with the perioperative team and fosters open dialogue regarding the best interests of the patient. The patient must also be included in the preplacement discussion so he or she can be truly informed and will not be distressed if he or she emerges from anesthesia with additional monitors in place. The psychomotor skills involved in monitor placement can be mastered at varying speeds, depending on the difficulty of actual placement. Many novice practitioners will place most of their focus on these skills, so effective instruction mandates patience and a consistent, systematic approach to accepted techniques for monitor placement. In fact, deemphasizing the importance of these motor skills and highlighting the indications, risks, and benefits is more important, as most practitioners will become technically proficient with time. Most new anesthesia providers will learn on real patients by trial and error, but other devices exist for practicing the psychomotor skills necessary to achieve competency in a safe and effective environment that does not subject the patient to the practicing student during the early phase of the learning curve (see the section on full environment simulation later in this chapter). Safely placing invasive monitoring techniques will also require the teaching of anatomy with a consideration of potential placement sites, emphasizing the risks and benefits of the site selection. Sterile technique during invasive monitor placement will also need to be taught and stressed; a standardized approach using mannequins in a nonclinical environment is ideal. Patient comfort and safety should also be emphasized, as all monitors, whether invasive or noninvasive, carry with them some inherent risks and discomfort. One consideration that is often learned the hard way by novices is the importance of the ergonomics of an operating room. Emphasizing the importance of planning ahead for the particular facets of a surgery (e.g., properly positioning the monitoring cables before turning the head of the bed 180 degrees), or actual work environment (e.g., being able to fit an echocardiography machine next to the patient) helps the operating room run more efficiently and saves

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the new practitioner undue embarrassment and conflict in the operating room.

Intraoperative phase During the intraoperative period, monitors are active and interpretation of data becomes the main focus. Although a working knowledge of normal human physiology underlies all successful monitor interpretation, many other facets of monitoring must be taught “on the job.” The technology behind a particular monitor and its inherent strengths, weaknesses, and corroborating, conflicting, or interfering factors are necessary pieces of information for the novice anesthesiologist to understand if he or she is to trust the data seen. An experienced practitioner can help novices develop and target these factors so when data deviate from normal or expected values, technical influences can quickly be ruled out and pathophysiologic sources of abnormal data can be pursued and corrected. Therapeutic interventions based on monitoring data rely on the data being correct; therefore, the gravity of intervening or not intervening must be emphasized. Teaching new practitioners to be vigilant is a component of monitoring not to be overlooked by educators. The conventional wisdom is that vigilance cannot be taught and will develop over time. Many novices experience information overload when they are first immersed in the operating room. A systematic approach (e.g., scanning the anesthetizing environment periodically by starting at the patient and making one’s way back to the machine and monitor) is learned more easily if it is taught explicitly. This gives a framework for vigilance and can then be modified as new practitioners become more experienced. In times of stress, inexperienced practitioners may rely on simple strategies to make disordered situations more manageable. In this way, teaching vigilance may increase patient safety by allowing the novice to make difficult decisions and interpretations in a distracting and demanding environment.

Postoperative phase Postoperative monitoring depends on similar factors considered in the preoperative phase. One crucial component is the predetermined definition of stability after the procedure is finished. Based on the patient’s state after the surgery, monitors are discontinued or new ones are placed and the patient’s destination (e.g., intensive care unit versus home) is determined.

Role of simulation in teaching monitoring skills The use of patient simulation to educate and evaluate providers of anesthesia (traditionally, anesthesiology residents) has become increasingly accepted. Although anesthesiology took the initiative in incorporating simulation into its culture, its use in education and evaluation has been widely embraced during the last two decades by both medical schools and

Chapter 4 – Teaching Monitoring Skills

postgraduate training programs. The American Board of Anesthesiology (ABA) now requires simulator-based education to fulfill maintenance of certification in anesthesia (MOCA) requirements,8 and the ACGME has recognized simulation as a useful assessment tool.9 The Israeli Board of Anesthesiology Examination Committee has given some primacy to simulation as an element in credentialing and certifying anesthesiologists.10 Indeed, the role of simulation appears to be evolving from that of an educational adjunct to an additionally useful tool in the assurance of clinical competence. Because monitoring skills are most important in dynamic perioperative settings, it follows that being trained in similar fashion would be beneficial. Hence, simulator-based education and evaluation are uniquely suited to this scope of anesthesia-based practice.

History and classification of medical simulation Although an exhaustive review of the history of medical simulation is beyond the scope of this chapter, a brief overview is in order. Cooper and Taqueti give a comprehensive survey of simulation and note that because the field is arguably in its infancy, few accepted conventions exist.11 Some basic terms with which the reader should be familiar are listed in Table 4.2. These definitions provide a broad framework with which to describe the various types of simulators available in medical education today and encompass a wide array of human (e.g., standardized patients) and manufactured (e.g., mannequins) simulation techniques. A more extensive system of classification has been described by Cumin and Merry.12 Inspired by the aviation industry, the first mannequin-based medical simulators were introduced in the early 1960s. ResusciAnne, designed by Asmund Laerdal, was developed during this time to teach mouth-to-mouth resuscitation. The concept of basic life support training using a mannequin-based simulator would grow out of this simple design as Laerdal partnered with Peter Safar, a Baltimore anesthesiologist, to enhance his simulator’s capabilities and realism.13 The model did not undergo significant improvement until the 1990s, when more anatomically correct airway features were added and the model was renamed SimMan, which is still commercially available.14

Table 4.2.

Common definitions in simulation

Term

Definition

Simulator

Any object or representation of the full or part task to be replicated Application of simulator to training and/or assessment Recreation of actual environment in which tasks are to be performed (e.g., OR, ICU) Technologies that replicate only a portion of a process or system The nearness to “true life” achieved by simulation

Simulation Immersive simulation Part-task simulation Fidelity

Adapted from reference 4.

Table 4.3.

Features of the HPS by METI

1. Pupils that automatically dilate and constrict in response to light 2. Thumb twitch in response to a peripheral nerve stimulator 3. Automatic recognition and response to administered intravenous and inhaled drugs and drug dosages 4. Variable lung compliance and airway resistance 5. Real-time oxygen consumption and carbon dioxide production 6. Automatic response to cardiovascular conditions, including ischemia needle decompression of a tension pneumothorax, chest tube drainage, and pericardiocentesis 7. Automatic control of urine output Adapted from www.meti.com.

Computer-driven simulators were first developed in the mid-1960s with SimOne, a full-scale mannequin with a chest capable of rise-and-fall action during respiration, blinking eyes, and a jaw that could open and close.15 A single SimOne was manufactured and was eventually lost to obscurity largely because it was ahead of its time, despite the fact that residents trained on the simulator acquired airway management skills more quickly than their colleagues. The Harvey cardiology mannequin was also developed in the 1960s but, unlike the Sim One, it has had sustainable use to the present day. This simulator is capable of a wide array of cardiac disease scenarios, has been researched and validated extensively and has evolved over time to include multimedia programs that enhance its fidelity.16–18 The development of mathematical modeling programs for human physiology and drug pharmacodynamics and pharmacokinetics led to the development of modern mannequin and screen-based simulators. Various evolutions of these mathematically driven simulators have been developed at Stanford and University of Florida Gainesville and are described elsewhere.4,19 Today the Human Patient Simulator (HPS), based on the Gainesville simulator and now manufactured by Medical Education Technologies Inc. (METI), is the prototypical fullscale, mathematical–model-driven product. This simulator can be used to stage full-scale simulations whereby realistic monitoring, physiologic response to drugs, and high-fidelity pathologic conditions can be encountered by participants. Key features of the HPS are listed in Table 4.3.20 A simple classification system of simulator types uses three categories: part-task trainers, computer-driven mannequins, and virtual reality simulators, on a continuum from low to high fidelity.21 Part-task trainers usually represent anatomical parts for teaching and/or evaluating skills (e.g., central line placement trainers for practicing sterile technique, landmark identification, and monitor placement and suturing) and are generally passive, noncomputerized models. However, part-task does not imply less sophisticated technology; more advanced parttask trainers have been designed, such as the various transesophageal echocardiography simulators. These simulators also include cursory responses to noxious stimuli, including audible sounds of discomfort from the “patient,” increased heart rate, and blood pressure, along with the ability to administer medications commonly used for sedation.

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Computer-driven mannequins, or realistic patient simulators (RPSs), possess anatomic features and process advanced pharmacologic and physiologic models to respond to stimuli and medication administration. Such mannequins are ideally suited for immersive and full environment simulation (FES), in which individuals or entire teams of health care providers can perform tasks, manage potentially deadly scenarios, and improve skills, including leadership, communication, delegation, and prioritization.22–25 Virtual reality (VR) simulations are the newest types of simulator, in which a computer-driven scenario is created and the user can interact with all the elements of the scenario. Visual, auditory, and haptic (touch and pressure) feedback are all available in VR simulations, but much work needs to be done to incorporate VR technology into the field of medical simulation.

General uses and benefits of simulated patients The growing interest in medical simulation for education and assessment of physicians has been fueled by many of the same factors that led to the use of simulation in the aviation and nuclear industries.26 The importance of simulation is evident in aviation, in which commercial pilots take their first flight only after a rigorous simulation program. The extensive use of simulation in the aviation industry has been driven not purely by evidence, but also by intuition and common sense. To date there is a lack of convincing evidence that simulator training improves health care education, practice, and patient safety, but, Gaba argues, “no industry in which human lives depend on skilled performance has waited for unequivocal proof of the benefits of simulation before embracing it.”27 Certainly, adopting simulation for the training in monitoring skills seems logical. An educational imperative is one obvious utility of simulation. Simulation is learner-centered in that the participant’s education receives highest priority. There exist no competing patient needs; therefore, the participant is afforded a unique opportunity to perform tasks without the looming stress of medical error. Medical clerkships and residency training rely on apprentice-based, chance encounters in which learning time is limited and not standardized. Simulation eliminates these limitations and, in doing so, benefits teachers by allowing for an optimal learning environment and a predesigned curriculum that emphasizes points deemed germane by the teacher. Also, presentation of uncommon but critical situations in which a rapid intervention is required is possible. This offers the learner the benefit of experience with a particular disease state in a safe environment rather than a purely “textbook” knowledge of the subject. Full environment simulation, in particular, allows for assessment and education that extends beyond simple cognitive measures. A participant or team of participants can be evaluated and trained in domains of clinical knowledge, communication, and teamwork and procedural and technical skills in one environment and in one simulation session. An expert

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for the domain(s) of interest can then debrief the participant(s).28 Debriefings are vital, as one can learn from mishaps that occurred during a scenario and also speak openly about perceived and actual errors and limitations without fear of liability, blame, or guilt. Errors are deliberately allowed to occur and reach their end, whereas in real life, a more capable clinician would necessarily be called. In this way, participants can see the results of their choices. Patient safety and medical errors have come to the forefront of health care since the Institute of Medicine released To Err is Human: Building a Safer Health System in 2000.29 The effective integration of simulation into medical education and assessment can address this modern health care challenge. In addition to the more obvious and intended benefits of simulation, the ethical benefits are also pronounced. Patients entrust health care providers with their well-being and enter into a relationship in which they believe their providers to be expertly trained. It follows that being trained in simulated scenarios before a real patient encounter reduces a patient’s exposure to less-seasoned professionals. Thus, patients theoretically receive a higher quality of care than they might otherwise get from those trained in apprentice-based systems, in which the adage of “see one, do one, teach one” may in fact overestimate the experience the provider has attained. As alluded to previously, other high-risk fields, such as aviation and the nuclear power industry, have adopted simulation in training personnel to acquire skills and knowledge and prove competency.30,31

Utility of simulation for monitoring skills development A formalized teaching philosophy with regard to monitor skills is lacking in many, if not most, medical education curricula. An understanding of human physiology is essential if one is to be adept at the science of monitoring, which is, in fact, a form of applied physiology. In the most traditional sense, physiology has been, and still is, taught to students throughout the world in the classroom. The emphasis on linear thinking (i.e., teaching a single concept at a time) helps learners digest complex information. However, complex human processes do not function in linear fashion and, although this setting has served numerous clinicians well since the advent of modern medical education, the past 20 years have seen the rise of new educational techniques to replace or augment this approach. Simulation provides an ideal format for teaching the attitudes, skills, and knowledge needed in monitoring. As defined by Gaba, “simulation is a technique—not a technology—to replace or amplify real experiences with guided experiences that evoke or replicate substantial aspects of the real world in a fully interactive manner.”32 Simulation enables both teacher and learner to engage in bedside teaching outside of the clinical setting with no patient risk, and creates an ideal environment for adult learning. One reason simulation has become more prominent in medical education is that modern medicine requires the move from

Chapter 4 – Teaching Monitoring Skills

theory to practice to occur faster than in the past. The health care industry has changed markedly and, in turn, medical education has had to evolve.33 Shorter hospital stays, a generally sicker hospitalized patient population, and greater legal concerns have decreased the number of patients a medical student is likely to encounter during his or her training.34 Simulation permits students and residents to function in an environment in which no actual patients can be harmed. At many medical schools, the traditional subject-based basic sciences are being replaced by system-based teaching. Lectures are often replaced or augmented by problem-based learning and small-group discussions regarding hypothetical, simulated case scenarios.35 In essence, simulation of patients is superseding the traditional teaching of pathophysiology. Building on the history of simulation in the aviation and defense industries, computerbased simulations and full-body human patient simulators now augment traditional medical education. In similar fashion, simulation techniques are necessarily assuming important roles in teaching more advanced concepts, such as monitoring skills. In a simulated environment, monitor skills can be taught as “pieces of a puzzle” that can be mastered individually. Monitor selection, monitor placement, monitor interpretation, data corroboration, monitor failure, data analysis, and medical management can each be taught in a standardized, digestible fashion without the time pressure or variability of the actual clinical environment. Only after mastery of each “piece” can the student then synthesize the “pieces” to formulate the entire “puzzle” of a simulated full-scale clinical environment. The chronological model outlined in the beginning of this chapter can be applied using FES and allows new anesthesia providers to practice the important components of the monitoring process. Using FES, an instructor can recreate an operating room setting using real patient monitors attached to a highfidelity mannequin simulator patient. An important benefit of FES is that the scenario can be tailored to the type and level of the learner. This is the key advantage of simulation education over traditional medical education that relies on chance encounters with relatively rare clinical situations for monitoring skills to be observed, learned, or practiced. The preoperative phase can be simulated with a standardized patient or actor playing the patient. This allows the participant in the FES to elicit a history and physical and review any lab data. Monitor placement can even be practiced at this point, using task-trainers set up in the FES. The learner can practice the psychomotor tasks needed in monitor skills, be exposed to rare events related to monitor malfunction or adverse medication reactions, and understand difficult-to-conceptualize topics such as monitor ergonomics. At each phase in the simulation, the learner can be asked about his or her rationale in choosing a particular monitor, as well as any other important points the educator seeks to review, such as theory behind the monitor, technology, and the like. Simulation also allows the teacher to assess learner performance and knowledge using reproducible clinical encounters rather than through standardized exams, which often require only the memorization of facts.

As the scenario moves to the intraoperative phase, data can be manipulated to teach proper interpretation, corroboration, and intervention based on different deviations from normal values. The use of FES acknowledges that monitoring data are not interpreted in a quiet or isolated environment, but in a stressful and often dizzying workplace. This adds an element of difficulty in the interpretation of data; FES provides an opportunity to practice vigilance, as well as cognitive and social skills, allowing learners to “think on their feet” in an environment fraught with demands and distractions. This makes good sense, considering that adult learners thrive in environments that are participative and interactive. This kind of contextual learning also allows the practitioner to experience the demands of monitor interpretation within an environment similar to what he or she will be experiencing in the actual operating room. The postoperative phase provides another opportunity to review the rationale behind any plans to continue or discontinue the monitors chosen at the start of the scenario. At the end of the simulation, a videotape of the learner’s performance can be reviewed and a debriefing with experienced practitioners can take place, something that is virtually impossible to do in actual practice and that is crucial for adult learners (i.e., immediate feedback). This opportunity to assess a learner’s monitoring skills using FES is superior to that offered in an operating room setting, where distractions and important patient care duties abound. Although the resources required to run a successful simulation program are possibly prohibitive at many centers, the potential benefits are apparent. The opportunity to teach nuances of monitoring skills is unparalleled and takes reliance on chance encounters with rare clinical situations out of the equation. The numerous advantages and disadvantages of simulation are listed in Table 4.4.36 Simulation need not occur on a grand scale such as FES, but may use simple screen-based simulators with continuous feeds

Table 4.4. Advantages/disadvantages of simulation as an educational technique36 Advantages No actual patient is threatened Standardized educational experience for each student Learner-centered, instructor-controlled Can be paused for reflection and correction Complex environment with multiple problems can be presented Rare situations can be reliably reproduced and practiced Interactive Immediate feedback Leadership and communication skills can be practiced Psychomotor skills can be taught and practiced Sessions can be recorded and reviewed after completion Disadvantages Expensive to start, house, and maintain simulation curriculum Only small groups of learners can be accommodated Performance anxiety may hinder learning Time required for preparing scenarios Learner may anticipate problems and be hypervigilant Source: From reference 36.

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of monitoring data. Such simulations may be best suited to lessadvanced practitioners acquiring a foundation of skills. However, for the high-stakes interpretation of monitors involved in anesthesiology, FES seems best suited to practicing true-to-life skills. Simulation not only should be thought of as a tool to educate new trainees, but can also serve practicing anesthesiologists and their educational needs. Of particular interest is the use of fullscale simulators to allow practicing health care providers the opportunity to learn and perfect clinical skills and techniques not available or mastered during training. Medical technology has expanded, and is anticipated to continue to expand, exponentially. It is likely that new and novel monitoring technologies will be introduced into the practice of anesthesiology. The fullscale simulated environment is ideal for anesthesiologists to practice and familiarize themselves with new technology without sacrificing operating room efficiency or patient safety. As patient care environments become increasingly complex, it becomes necessary for practitioners to use equally complex modalities of monitoring to optimize patient care. The rapid pace of monitor development often supersedes the time available to trainees and practitioners that is necessary to learn new monitor skills or refresh facility with extant ones. Complexity, increased demand to practice efficiently, and the demand to reduce patient errors have made the actual clinical environment less conducive for education. Gone are the days when the educational dictum of “see one, do one, teach one” was law. Modern educational programs will need to promote the use of multimodality formats to enhance learning, protect patients during the learning process, and create sustained skill acquisition in practicing anesthesiologists. The availability of new educational technology, such as computers, virtual reality, and mannequin-based simulators, will support such endeavors. Here we describe one possible teaching module that fosters the use of multimodality formats and simulation-based technology that addresses the needs of students in an efficient, learnercentered way that protects patients now and in the future.

References 1. http://www.acgme.org/acWebsite/RRC 040/040 prIndex.asp. 2. Bryan R, Kreuter M, Brownson R. Integrating adult learning principles into training for public health practice. Health Promotion Practice. 2008;10(4):557–563. 3. Davis, D et al. Impact of formal continuing medical education: do conferences, workshops, rounds and other traditional continuing education activities change physician behavior or health care outcome? JAMA 1999;282(9):867–874. 4. Gercenshtein L, Fogelman Y, Yaphe J. Increasing the satisfaction of general practitioners with continuing medical education programs: A method for quality improvement through increasing teacher-learner interaction. BMC Family Prac 2002;3:15–19. 5. Cantillion P, Jones R. Does continuing medical education in general practice make a difference? Br Med J 1999;318:1276–1279. 6. Reiter HI, Eva KW, Hatala RM, Norman GR. Self and peer assessment in tutorials: application of a relative-ranking model. Acad Med 2002;77:1134–1139.

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7. 6 http://www.acgme.org/outcome/comp/compMin.asp. 8. American Board of Anesthesiology: http://www.theaba.org/ anes-moc.asp. 9. Toolbox of Assessment Methods 2000. Accreditation Council for Graduate Medical Education (ACGME), and American Board of Medical Specialties (ABMS). Version 1.1. 10. Ziv A, Rubin O, Sidi A, Berkenstadt H. Credentialing and certifying with simulation. Anesthesiol Clin 2007;25:261–269. 11. Cooper JB, Taqueti VR. A brief history of the development of mannequin simulators for clinical education and training. Qual Saf Health Care 2004;13(Suppl1):i11–i18. 12. Cumin D, Merry AF. Simulators for use in anaesthesia. Anaesthesia 2007;62:151–162. 13. Grevnik A, Schaefer JJ. From Resusci-Anne to Sim Man: The evolution of simulators in medicine. Crit Care Med 2004;32:556–557. 14. Schaefer J, Gonzalez R. Dynamic simulation: a new tool for difficult airway training of professional healthcare providers. Am J Clin Anesth 2000;27:232–242. 15. Denson J, Abrahamson S. A computer-controlled patient simulator. JAMA 1969;208:504–508. 16. Gordon MS. Cardiology patient simulator: development of an automated manikin to teach cardiovascular disease. Am J Cardiol 1974;34:350–355. 17. Issenberg SB, Gordon MS, Gordon DL, et al. Simulation and new learning technologies. Med Teach 2001;23:16–23. 18. Sajid AW, Ewy GA, Felner JM, et al. Cardiology patient simulator and computer-assisted instruction technologies in bedside teaching. Med Educ 1990;24:512–517. 19. Gaba DM, DeAnda A. A comprehensive anesthesia simulation environment: recreating the operating room for research and training. Anesthesiology 1988;69:387–394. 20. METI: http://www.meti.com. 21. Scalese RJ, Obeso VT, Issenberg SB. Simulation technology for skills training and competency assessment in medical education. J Gen Intern Med 2007;23(Suppl 1):46–49. 22. Howard SK, Gaba DM, Fish KJ, et al. Anesthesia crisis resource management training: Teaching anesthesiologists to handle critical incidents. Aviat Space Environ Med 1992;63: 763–770. 23. Gaba DM, Fish KJ, Howard SK. Crisis Management in Anesthesiology. New York: Churchill Livingstone, 1994. 24. Holzman RS, Cooper JB, Gaba DM, et al. Anesthesia crisis resource management: Real-life simulation training in operating room crises. J Clin Anesth 1995;7:675–687. 25. Gaba DM, Howard SK, Fish KJ, et al. Simulation-based training in anesthesia crisis resource management (ACRM): A decade of experience. Simul Gaming 2001;32:175–193. 26. Ziv A, Small SD, Wolpe PR. Patient safety and simulation-based medical education. Med Teach 2000;22(5):489–495. 27. Gaba DM. Improving anesthesiologists’ performance by simulating reality. Anesthesiology 1992;76:491–494. 28. Issenberg SB, McGaghie WC, Petrusa ER, et al. Features and uses of high-fidelity medical simulations that lead to effective learning: a BEME systematic review. Med Teach 2005;27(1):10–28. 29. Institute of Medicine. To Err is Human: Building a Safer Healthcare System. Washington DC: National Academy Press, 2000. 30. Goodman W. The world of civil simulators. Flight Intl 1978;18:435. 31. Wachtel J. The future of nuclear power plant simulation in the United States. In: Simulation for Nuclear Reactor Technology.

Chapter 4 – Teaching Monitoring Skills

Walton DG (ed.). Cambridge: Cambridge University Press, 1985:339–349. 32. Gaba DM. The future vision of simulation in health care. Qual Saf Health Care. 2004;13 Suppl 1:i2–i10. 33. Richardson WC, et al. Crossing the Quality Chasm: A New Health System for the 21st Century. Washington, DC: National Academy Press, 2000.

34. Mardis R, Brownson K. Length of stay at an all time low. Health Care Manager 2003;22:122–127. 35. Shokar G, Shokar N, Romero C. Self-directed learning: looking at outcomes with medical students. Fam Med 2002;34:197–200. 36. Rauen CA. Simulation as a teaching strategy for nursing education and orientation in cardiac surgery. Crit Care Nurse 2004;24(3):46–51.

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Chapter

5

Electrocardiography Alexander J. C. Mittnacht and Martin London

Introduction Electrocardiography (ECG) monitoring and interpretation are considered part of the basic or minimal monitoring requirements in all patients undergoing diagnostic and/or therapeutic procedures, regardless of the anesthesia technique administered. The American Society of Anesthesiologists (ASA) guidelines for basic anesthesia monitoring, available online at http://www.asahq.org/publicationsAndServices/standards/02. pdf (last amended October 2005), mandate continuous ECG monitoring for the evaluation of a patient’s circulation during all anesthetics from the beginning of anesthesia until preparing to leave the anesthetizing location. The ASA guidelines also state that under extenuating circumstances, the responsible anesthesiologist may waive ECG monitoring, but recommends that when this is done, the anesthesiologist should leave a note in the patient’s medical record, excluding the reason for not excluding ECG monitoring. Consequently, all practitioners involved in perioperative patient care should have at least a basic understanding of ECG monitoring. With advances in computer technology, the diagnostic and monitoring capabilities of the ECG for the detection of arrhythmias and myocardial ischemia and infarction continue to develop and expand, and the distinction between diagnostic ECG carts and bedside ECG monitoring units is narrowing. The universal availability of affordable digital storage allows for almost continuous recording of large amounts of perioperative data, including information derived from ECG monitoring. The ability to retrieve such ECG data can serve as invaluable information in analyzing perioperative cardiac events. Although it seems obvious that patients should benefit from continuous ECG monitoring, evidence-based medicine would require proof of improved patient outcome, preferably including data from several large randomized prospective studies. However, given the stated ASA recommendations, randomizing patients to ECG monitoring would be nearly impossible. The American Heart Association (AHA) has published practice standards for ECG monitoring in hospital settings. Based mostly on expert opinion, recommendations are given regarding cardiac arrhythmia, ischemia, and QT interval ECG monitoring.1 Furthermore, the most recent American College of Cardiology/AHA Task Force on Practice Guidelines in patients

36

undergoing noncardiac surgery include recommendations on pre- and postoperative 12-lead ECG monitoring.2 The following text is intended not to be a substitute for extensive cardiology textbooks written on ECG monitoring, but rather to provide the practitioner involved in patient anesthesia care with a basic understanding of ECG monitoring requirements and ECG interpretation, as well as an overview of recent developments and available data on ECG monitoring and patient outcome.

Technical concepts Historical perspective Willem Einthoven is universally considered the father of electrocardiography (for which he won the 1924 Nobel Prize). However, Augustus Waller actually recorded the first human ECG in 1887, using a glass capillary electrometer. This early device used changes in surface tension between mercury and sulfuric acid in a glass column induced by a varying electric potential. The level of the meniscus was magnified and recorded on moving photographic paper, describing what were initially termed “A– B–C–D waves.” In 1895, Einthoven published his observations using this crude device. Frustration with its low-frequency resolution led him to develop the string galvanometer, using a silvercoated quartz fiber suspended between the poles of a magnet. Changes induced by the electrical potentials conducted through the quartz string resulted in its movement at right angles to the magnetic field. The shadow of the string, backlit from a light source, was transmitted through a microscope (the string was only 2.1 mm in diameter) and was recorded on a moving photographic plate. He renamed the signal the P–QRS–T complex (based on standard geometric convention for describing points on curved lines). Many of the basic clinical abnormalities (i.e. bundle-branch block, delta waves, ST-T changes with angina) in electrocardiography were first described using the string galvanometer. It was used until the 1930s, when it was replaced by a system using vacuum tube amplifiers and a cathode ray oscilloscope. A portable direct-writing ECG cart was not introduced until the early 1950s (facilitated at first by transistor technology and subsequently by integrated circuits), which allowed widespread use

Chapter 5 – Electrocardiography

of the ECG in clinical practice. The first analog-to-digital (A/D) conversion systems for the ECG were introduced in the early 1960s, but their clinical use was restricted until the late 1970s. Today, with advances in microcomputer technology, most ECG machines convert the analog ECG signal to digital form before further processing.

Power spectrum of the ECG The ECG signal must be considered in terms of its amplitude (or voltage) and its frequency components (generally termed its phase). The power spectrum of the ECG is derived by Fourier transformation, in which a periodic waveform is mathematically decomposed to its harmonic components (sine waves of varying amplitude and frequency). The frequency of each of these components can be equated to the slope of the component signal. The R wave, with its steep slope, is a high-frequency component, whereas the P and T waves have lesser slopes and are lower in frequency. The ST segment has the lowest frequency, not much different from the underlying electrical (i.e. isoelectric) baseline of the ECG. Prior to the introduction of digital signal processing (DSP), accurately displaying the ST segment presented significant technical problems, particularly in operating room (OR) and ICU bedside monitoring units (discussed later). Although the overall frequency spectrum of the QRS complex in Figure 5.1 does not appear to exceed 40 Hz, many components of the QRS complex, particularly the R wave, exceed 100 Hz. Thus, reducing the ECG signal to a bandwidth between 0.5 Hz and 40 Hz (monitoring mode) reduces artifacts but is unacceptable for diagnostic purposes (diagnostic mode 0.05–150 Hz; also see discussion later). Very high-frequency signals of particular clinical significance are pacemaker spikes. Their short duration and

high amplitude present technical challenges for proper recognition and rejection to allow accurate determination of the heart rate (HR). Spectra representing some of the major sources of artifact must be eliminated during processing and amplification of the QRS complex.

Frequency response of ECG monitors: monitoring and diagnostic modes Given the importance of the ECG in diagnosing myocardial ischemia, it is important to realize that significant ST segment depression or elevation can occur solely as a result of improper ECG signal filtering.3 This was a particular problem prior to the introduction of DSP. The AHA Electrocardiography and Arrhythmias Committee released specific recommendations regarding ECG signal sampling, filtering, and further processing.4,5 To reproduce the various frequencies components accurately, they all must be amplified equally. Thus, the monitor must have a flat amplitude response over the wide range of frequencies present. Similarly, because the slight delay in a signal as it passes through a filter or amplifier may vary in duration with different frequencies, all frequencies must be delayed equally. This is termed linear phase response. If the response is nonlinear, various components may appear temporally distorted (termed phase shift). The AHA recommends a bandwidth from 0.05 Hz to 150 Hz (250 Hz for children) for all 12lead diagnostic ECGs. A low-frequency cutoff of 0.5 Hz and a high-frequency cutoff of 40 Hz is commonly referred to as a monitoring mode. This produces a more stable signal with less baseline noise and fewer high-frequency artifacts. According to the most recent AHA recommendations, ECG machines should alert the user when used in the monitoring mode. Because most newer monitors use signal-averaging techniques that effectively eliminate most artifacts even in the diagnostic mode, the clinician can usually (and should) avoid using the monitoring mode whenever possible.

Intrinsic and extrinsic artifacts

Figure 5.1. The typical power spectrum of the electrocardiography (ECG) signal, including its subcomponents and common artifacts (motion and muscle noise). The power of the P and T waves (P–T) is low-frequency, and the QRS complex is concentrated in the mid-frequency range, although residual power extends up to 100 Hz. From Thakor NV et al. Estimation of QRS complex power spectra for design of a QRS filter. IEEE Trans Biomed Eng 1984;31(11):702–6 (Figure 4), with permission.

ECG artifacts and baseline wander may result from several causes.6–11 Even though the development of DSP techniques has helped to minimize these artifacts, new sources of electrical interference have emerged. Implantable, miniaturized devices such as neurostimulators, pacemaker/defibrillators, and infusion pumps are almost unrecognizable, and artifacts resulting from such devices must be carefully evaluated and correctly interpreted. Table 5.1 lists more common causes of such artifacts. To avoid or minimize such artifacts, signal acquisition should be optimized. Proper electrode application and positioning are simple methods in improving ECG quality. Monitoring electrodes should preferentially be placed directly over bony prominences of the torso (i.e. clavicular heads and iliac prominences) to minimize excursion of the electrode during respiration, which could cause baseline wander. Electrode impedance must be optimized to avoid loss and alteration of the signal.

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Monitoring in Anesthesia and Perioperative Care

Table 5.1.

Common causes of ECG artifacts

- Skin impedance - ECG electrodes, cables - Electromyographic (EMG) noise (motor activity) - Electrical power line interference, line isolation monitor (LIM) - Electrocautery - Evoked potential monitoring - Mechanical ventilation - Magnetic resonance imaging (MRI) - Extracorporeal shock wave lithotripsy (ESWL) - Neurostimulators, implantable infusion pumps - Infusion pumps, blood warmers - Extracorporeal blood circulation devices, such as cardiopulmonary bypass devices and renal replacement therapy

By removing a portion of the stratum corneum (gentle abrasion with a dry gauze pad, resulting in a minor amount of surface erythema, works well), skin impedance can be reduced by a factor of 10 to 100. Optimal impedance is 5000 ohms or less. The electrode may be covered with a watertight dressing to prevent surgical scrub solutions from undermining electrode contact. To minimize electrocautery artifact, the right leg reference electrode should be placed as close as possible to the grounding pad, and the ECG monitor should be plugged into a different power outlet than the electrosurgical unit. Devices with which the patient is in physical contact, particularly via plastic tubing, may at times cause clinically significant ECG artifacts. Although the exact mechanism is uncertain, two leading explanations are either a piezoelectric effect caused by mechanical deformation of the plastic, or buildup of static electricity between two dissimilar materials, especially those in motion. This effect has been (a)

(b)

(c)

38

noted with the use of cardiopulmonary bypass, renal replacement therapy, and the like and usually mimics atrial arrhythmias (also see Figure 5.2). A grounding lead on the external device usually eliminates this.

Lead systems Where and how ECG electrodes are placed on the body is a critical determinant of the morphology of the ECG signal. Lead systems have been developed based on theoretical considerations (i.e. the orthogonal arrangement of the Frank XYZ leads) and/or references to anatomic landmarks that facilitate consistency between individuals (i.e. standard 12-lead system).

History and description of the 12-lead system Einthoven established electrocardiography using three extremities as references: the left arm (LA), right arm (RA), and left leg (LL). He recorded the difference in potential between the LA and RA (lead I), LL and RA (lead II), and LL and LA (lead III). Because the signals recorded were differences between two electrodes, these leads were termed bipolar. The right leg (RL) served only as a reference electrode. Einthoven postulated that the three limbs defined an imaginary equilateral triangle with the heart at its center. Because Kirchoff ’s loop equation states that the sum of the three voltage differential pairs must equal zero, the sum of leads I and III must equal lead II (which is therefore redundant). Given the influence of Einthoven’s vector analyses of frontal plane forces, others eventually incorporated the other two orthogonal planes (transverse and sagittal). Figure 5.2. Artifactual atrial flutter during continuous venovenous hemofiltration. (a) Initial 12-lead electrocardiogram during hemofiltration; (b) rhythm strip at time hemofiltration was turned off (black arrow); (c) rhythm strip with flow rate of filtration system decreased by half. Kaltman JR, Shah MJ. Artefactual atrial flutter. Cardiol Young 2006;16:195–196 (Figure 1), with permission.

Chapter 5 – Electrocardiography

Wilson refined and introduced the unipolar precordial leads into clinical practice. To implement these leads, he postulated a mechanism whereby the absolute level of electrical potential could be measured at the site of the exploring precordial electrode (the positive electrode). A negative pole with zero potential was formed by joining the three limb electrodes in a resistive network in which equally weighted signals cancel each other out. He termed this the central terminal, and in a fashion similar to Einthoven’s vector concepts, he postulated that it was located at the electrical center of the heart, representing the mean electrical potential of the body throughout the cardiac cycle. He described three additional limb leads (VL, VR, and VF). These leads measured new vectors of activation; thus, the hexaxial reference system for determination of electrical axis was established. Wilson subsequently introduced the six unipolar precordial V leads in 1935.12 Clinical application of the unipolar limb leads was limited because of their significantly smaller amplitude relative to the bipolar limb leads from which they were derived. They were not clinically applied until Goldberger augmented their amplitude (by a factor of 1.5) by severing the connection between the central terminal and the lead extremity being studied (which he termed augmented limb leads) in 1942. The three limb leads (I, II, and III), the three augmented limb leads (aVR, aVL, and aVF), and the six precordial leads (V1 through V6) have been universally accepted as the conventional 12-lead ECG system. However, in the AHA’s most recent recommendations for the standardization and interpretation of the ECG, the use of the terms “unipolar” and “bipolar” is discouraged and should be avoided, as all leads are effectively bipolar.13 Additional lead systems, and other expanded and derived lead systems, have been developed for specific clinical applications. The EASI-derived 12-lead ECG system is a based on vectorcardiography,14 and uses fewer electrodes (four chest electrodes and one reference electrode) and well-defined convenient landmarks (see Figure 5.3). The EASI system has been shown to compare favorably with the standard 12-lead ECG system for ischemia and arrhythmia detection and offers advantages in long-term continuous patient monitoring (e.g., fewer electrodes, increased patient comfort, less interference with patient care).15–19 At this point, the AHA does not recommend derived lead systems as a substitute for standard 12-lead (10 electrodes) ECGs.13 Figure 5.3. Location of the four EASI electrodes. A ground electrode can be placed anywhere on the body. From reference 17 (Figure 1), with permission.

B

I

A

E

Detection of myocardial ischemia Pathophysiology of ST segment responses The ST segment is the most important portion of the QRS complex for evaluating ischemia. The origin of this segment at the point where the QRS complex joins the ST segment (junction between QRS complex and ST segment or J point) may deviate from baseline in myocardial ischemia and is easy to locate. Its end, which is generally accepted as the beginning of any change of slope of the T wave, is more difficult to determine. In normal individuals, there may be no discernible ST segment, as the T wave starts with a steady slope from the J point, especially at rapid heart rates. The T–P segment has been used as the isoelectric baseline from which changes in the ST segment are evaluated, but, with tachycardia, this segment is eliminated and, during exercise testing, the P–R segment is used. The P– R segment is used in all ST segment analyzers as well. Repolarization of the ventricle proceeds from the epicardium to the endocardium, opposite to the vector of depolarization. The ST segment reflects the midportion, or phase 2, of repolarization, during which there is little change in electrical potential. Thus, it is usually isoelectric. Ischemia causes a loss of intracellular potassium, resulting in a current of injury. The electrophysiologic mechanism accounting for ST segment shifts (either elevation or depression) remains controversial. The two major theories are based on either a loss of resting potential as current flows from the uninjured to the injured area (diastolic current), or a true change in phase 2 potential as current flows from the injured to the uninjured area (systolic current). With subendocardial injury, the ST segment is depressed in the surface leads. With epicardial or transmural injury, the ST segment is elevated. When a lead is placed directly on the endocardium, opposite patterns are recorded.

ECG manifestations of ischemia With myocardial ischemia, repolarization is affected, resulting in downsloping or horizontal ST segment depression. Varying local effects and differences in vectors during repolarization result in different ST morphologies that are recorded by the different leads. It is generally accepted that ST changes in multiple leads are associated with more severe degrees of coronary artery disease (CAD). The classic criterion for ischemia is a 0.1 mV (1 mm) depression measured 60 to 80 msec after the J point. The slope of the segment must be horizontal or downsloping. Downsloping depression may be associated with a greater number of diseased vessels and a worse prognosis than horizontal depression. Slowly upsloping depression with a slope of 1 mV/sec or less is also used but is considered less sensitive and specific (and difficult to assess clinically). Nonspecific ST segment depression can be related to the use of drugs, particularly digoxin.20,21 Interpretation of ST segment changes in patients with left ventricular hypertrophy (LVH) is particularly controversial, given the tall

39

Monitoring in Anesthesia and Perioperative Care

R wave baseline, J point depression, and steep slope of the ST segment. The criteria for ischemia with ST segment elevation (≥ 0.1 mV in ≥ 2 contiguous leads) are used in conjunction with clinical symptoms or elevation of biochemical markers to diagnose acute coronary syndromes. ST segment elevation is usually caused by transmural ischemia, but may potentially represent a reciprocal change in a lead oriented opposite the primary vector with subendocardial ischemia (as may be seen in the reverse situation).22,23 Perioperative ambulatory monitoring studies have also included ⬎ 0.2 mV in any single lead as a criterion, but ST elevation is rarely reported in the setting of noncardiac surgery. It is commonly observed, however, during weaning from cardiopulmonary bypass (CPB) in cardiac surgery with relative frequency, and during coronary artery bypass graft (CABG) surgery (both on and off pump) with interruption of coronary flow in a native or graft vessel. ST elevation in a Q wave lead should not be analyzed for acute ischemia, although it may indicate the presence of a ventricular aneurysm. Despite the clinical focus on the ST segment for monitoring, the earliest ECG change at the onset of transmural ischemia is the almost immediate onset of tall and peaked (hyperacute) T waves, a so-called primary change. This phase is often transient. A significant increase in R wave amplitude may also occur at this time. T wave inversions (symmetrical inversion) commonly accompany transmural ST segment elevation changes, although the vast majority of T wave inversions and/or flattening observed perioperatively are nonspecific, resulting from transient alterations of repolarization caused by changes in electrolytes, sympathetic tone, and other noncardiac factors. Although repolarization changes (e.g. ST–T wave) have long been the focus of ischemia detection, it has been well documented that changes in the high-frequency (150–250 Hz) recordings of the QRS complex may be a more sensitive marker for ischemia.24 This effect is likely the result of slowing of conduction velocity in the ischemic region.25 Such changes are not visible on the standard ECG, and large intra- and interindividual variations in the high-frequency recordings of the QRS complex are present even in healthy individuals (also see Figure 5.4).26 Absolute changes in the root mean square (RMS) of measured QRS amplitudes ⬎ 0.6 ␮V or relative changes ⬎20 percent are considered clinically significant.27 Pettersson and colleagues documented a higher sensitivity of this approach compared with 12-lead ST segment analysis in the detection of acute coronary occlusion during percutaneous transluminal coronary angioplasty (PTCA).28 The overall sensitivity was 88 percent, compared with 71 percent using ST-segment elevation criteria, or 79 percent by combining ST-segment elevation and depression. Its greatest value was in the detection of circumflex and right coronary occlusions. Anesthesia induction also seems to change high-frequency ECG parameters; however, a small study found these changes to be within the described normal limits.29 Although intriguing, further studies are clearly required, and it is unlikely that high-frequency ECG analysis will be used commonly in the

40

(a) R 0.5 mV T

P Q

S 200 msec

(b)

5 μV

100 msec

5 μV

(c)

RAZ

100 msec

Figure 5.4. Twelve-lead high-frequency QRS electrocardiograms. (a) A conventional surface electrocardiogram signal from a healthy subject. (b) High-frequency QRS signal in a healthy individual in whom ECG signals were analyzed at a sampling rate of ⬎1000/s, signal-averaged, and then passed through a filter excluding frequencies outside a range of 150–250 Hz. Note the reduced voltage scale compared with trace (a). (c) High-frequency QRS signal from a patient with myocardial ischemia. There are two peaks in the envelope of the high-frequency QRS signal, rather than the single peak in trace (b). The dip in the envelope (arrow) is denoted as a reduced-amplitude zone (RAZ). From reference 29 (Figures 1–3), with permission.

near future, given the expense of replacing or upgrading existing equipment.

Perioperative ECG ischemia monitoring Detection of perioperative myocardial ischemia has received considerable attention over the past several decades and, more recently, with publication of several studies of clinical monitoring and therapy (e.g. perioperative beta blockade).30 Many of these studies demonstrated associations of perioperative ischemia with adverse cardiac outcomes in adults undergoing a variety of cardiac and noncardiac surgical procedures, particularly major vascular surgery.31–33 With regard to ECG devices, advances in ECG technology now allow for automated ST segment trend monitoring in almost all perioperative clinical settings. However, applying this technology routinely, even in low-risk surgical patients, may yield false-positive responses (although these are uncommon). Perhaps the bigger challenge is interpreting minor ST segment changes in the context of the overall risk profile of the patient. Recent studies document that transient myocardial

Chapter 5 – Electrocardiography

ischemia occurs in the absence of significant CAD in unexpected patients, such as parturients, particularly with significant hemodynamic stress and/or hemorrhage.34 Although the precise etiology of such changes is uncertain, significant troponin release has been recently documented in these patients, confirming the suspicion that these ECG changes are true ischemic responses (likely related to subendocardial ischemia owing to global hypoperfusion). The recommended leads for perioperative ECG monitoring, based on several clinical studies, do not differ substantially from those used during exercise testing, although considerable controversy as to the optimal lead(s) persists in both clinical settings. Early clinical reports of intraoperative monitoring using the V5 lead in high-risk patients were based on observations during exercise testing, in which bipolar configurations of V5 demonstrated high sensitivity for myocardial ischemia detection (up to 90%). Subsequent studies using 12lead monitoring (torso-mounted for stability during exercise) confirmed the sensitivity of the lateral precordial leads.35,36 Some studies, however, reported higher sensitivity for leads V4 or V6 compared with V5 , followed by the inferior leads (in which most false-positive responses were reported).37–44 With the widespread growth of percutaneous coronary intervention (PCI) for acute myocardial infraction and unstable angina in the 1990s, a number of investigators have reported on the use of continuous ECG monitoring (3 or 12 leads) in this setting. The controlled occlusion of specific coronary artery branches during PCI has extended our knowledge regarding vessel-specific ECG responses to acute myocardial ischemia. Horacek and Wagner found ST segment elevation in leads V2 and V3 to be most sensitive for occlusion of the left anterior descending artery, and leads III and aVF most sensitive for the right coronary artery.45 In contrast, circumflex occlusion results in variable responses, with primary elevation in the posterior precordial leads V7 through V9 (which are rarely monitored clinically), and reciprocal ST segment depression in the standard precordial leads (V2 or V3 ).46,47 For transmural ischemia, sensitivity is highest in the anterior rather than in the lateral precordial leads. The most widely quoted clinical study using continuous, computerized 12-lead ECG analysis in a mixed cohort (vascular and other noncardiac procedures) by London and coworkers reported that nearly 90 percent of responses involved ST segment depression alone (75% in V5 and 61% in V4 ).48 In approximately 70 percent of patients, significant changes were noted in multiple leads. When considered in combination (as would be done clinically), the use of both leads V4 and V5 increased sensitivity to 90 percent, whereas the standard clinical combination, leads II and V5 , was only 80 percent sensitive. Use of leads V2 through V5 and lead II captured all episodes (see Table 5.2). A larger clinical study by Landesberg and associates of patients undergoing vascular surgery using a longer period of monitoring (up to 72 hours) with more specific criteria for ischemia (⬎10 minute duration of episode) extended these observations. They reported that V3 was most sensitive for

Table 5.2. Sensitivity for different ECG lead combinations for intraoperative ischemia detection

Lead Combination 1 lead V5 2 leads 3 leads 4 leads

Sensitivity (%) II V4 75 II/V5 II/V4 V4 /V5 V3 /V4 /V5 II/V4 /V5 II/V2 –V5

33 61 80 82 90 94 96 100

Based on data presented in reference 48.

ischemia (87%) followed by V4 (79%), while V5 alone was only 66 percent sensitive (also see Figure 5.5).49 In the subgroup of patients for whom prolonged ischemic episodes ultimately culminated in infarction, however, V4 was most sensitive (83%). In this study, all myocardial infarctions were non–Q-wave events detected by troponin elevation. Use of two precordial leads detected 97 percent to 100 percent of changes. Based on analysis of the resting isoelectric levels of each of the 12 leads (a unique component of this study), it was recommended that V4 was the best single choice for monitoring of a single precordial lead, as it was most likely to be isoelectric relative to the resting 12-lead preoperative ECG. In contrast, the baseline ST segment was more likely above isoelectric in V1 –V3 and below isoelectric in V5 –V6 . Surprisingly, no episodes of ST elevation were noted in this study, as opposed to 12 percent in the earlier study of London and colleagues, in which such changes were noted in inferior and anteroseptal precordial leads. A multidisciplinary working group specifically recommends continuous monitoring of leads III, V3 , and V5 for all acute coronary syndrome patients.50 The coronary care unit’s use of continuous ECG monitoring has received increasing attention recently as well.51 Martinez et al. evaluated a cohort of vascular patients monitored in the ICU for the first postoperative day using continuous 12-lead monitoring using a threshold of 20 minutes for an ischemic episode.52 Eleven percent of patients (of 149 patients) met the criteria, with ST depression in 71 percent and ST elevation alone in 18 percent (12% with both). The majority of changes were detected in V2 (53%) and V3 (65%). Using the standard two-lead system (II and V5 ), only 41 percent of episodes would have been detected. Although these studies clearly support the value of precordial monitoring in patients at risk for subendocardial ischemia, one must be vigilant for the rare patient with acute Q-wave infarction (most commonly in the inferior leads). The use of multiple precordial leads, although appealing, is not likely to become common clinical practice, owing to the limitations of existing monitors (and cables). Even if such equipment were available, it is likely that considerable resistance would occur from practitioners because of the extra effort associated with this approach. Perhaps, in the future, when lower-cost wireless

41

Monitoring in Anesthesia and Perioperative Care

90

Percentage of the 12 ischemic events progressing to myocardial infarction, at peak ischemia

80 Incidence of leads with ST deviation

All leads with ST deviation 70

Figure 5.5. Histogram showing the incidence of all electrocardiographic leads, demonstrating greater than 1 mm relative ST deviation during peak ischemia and the electrocardiographic lead with the maximal ST deviation in 12 patients with myocardial infarction. From reference 49 (Figure 5), with permission.

Leads with maximal relative ST deviation

60 50 40 30 20 10 0

aVL

L1

-aVR

L2

aVF

L3

V1

V2

V3

V4

technologies are perfected, this approach may become a clinical reality.

Perioperative arrhythmia monitoring Heart rhythm diagnosis is one of the main features of perioperative ECG monitoring. Consequently, there has been considerable interest in the refinement of arrhythmia detection algorithms and their validation.53 Most modern ECG machines feature real-time automated computerized arrhythmia detection algorithms, allowing for the detection, audiovisual signaling, and recording of clinical relevant arrhythmias, including asystole, ventricular tachycardia/fibrillation, bradycardia, R on T, and irregular rhythm recognition. As expected, the devices’ accuracy for detecting ventricular arrhythmias is high but is much lower for detecting atrial arrhythmias. Typically, inferior ECG leads are preferred in rhythm diagnosis, allowing superior discrimination of the P wave morphology. Particularly in the OR setting, a variety of artifacts – for example, those caused by electrocautery – are common causes of false-positive responses. Aside from rhythm diagnosis, an increasing number of patients are presenting for surgery with a pacemaker or an automated implantable defibrillator (which also has a pacemaker function) implanted. The anesthesiologist should not only be familiar with the latest recommendations regarding perioperative management of patients presenting with such devices but should also be aware of possible interference with normal ECG monitoring. The detection of pacemaker spikes may be complicated by very-low-amplitude signals related to bipolar pacing leads, varying amplitude with respiration, and total body fluid accumulation.53 Most critical care and ambulatory monitors incorporate pacemaker spike enhancement for small high-

42

V5

V6

frequency signals (typically 5–500 mV with 0.5–2 ms pulse duration) to facilitate recognition. However, this can lead to artifacts if there is high-frequency noise within the lead system.

Summary ECG monitoring has been used for perioperative hemodynamic monitoring for more than four decades. Most of its basic features remain unchanged, although improvements in automated ischemia and arrhythmia detection have increased its clinical utility. It is relatively inexpensive, completely noninvasive, and can easily be used for continuous monitoring in every patient, extending into the postoperative setting. Unlike newer modalities, such as transesophageal echocardiography, that may have a higher sensitivity for ischemia detection, only basic training is necessary for most ECG monitoring purposes.

References 1. Drew BJ, Califf RM, Funk M, et al. Practice standards for electrocardiographic monitoring in hospital settings. An American Heart Association Scientific Statement from the councils on cardiovascular nursing, clinical cardiology, and cardiovascular disease in the young. Circulation 2004;110: 2721–46. 2. Fleisher LA, Beckman JA, Brown KA, et al. ACC/AHA 2007 guidelines on perioperative cardiovascular evaluation and care for noncardiac surgery: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 2002 Guidelines on Perioperative Cardiovascular Evaluation for Noncardiac Surgery). Anesth Analg 2008;106:685–712. 3. Kligfield P, Okin PM. Prevalence and clinical implications of improper filter settings in routine electrocardiography. Am J Cardiol 2007;99:711–3.

Chapter 5 – Electrocardiography

4. Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and interpretation of the electrocardiogram. Part I: the electrocardiogram and its technology, a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2007;49:1109–27. 5. Mason JW, Hancock EW, Gettes LS. Recommendations for the standardization and interpretation of the electrocardiogram. Part II: electrocardiography diagnostic statement list, a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society Endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2007;49:1128–35. 6. Patel SI, Souter MJ. Equipment-related electrocardiographic artifacts: causes, characteristics, consequences, and correction. Anesthesiology 2008;109:138–48. 7. McGrath B, Columb M. Renal replacement therapy causing ECG artefact mimicking atrial flutter. Br J Intensive Care 2004;14:49–52. 8. Marples IL. Transcutaneous electrical nerve stimulation (TENS): An unusual source of electrocardiogram artefact. Anaesthesia 2000;55:719–20. 9. Khambatta HJ, Stone JG, Wald A, Mongero LB. Electrocardiographic artifacts during cardiopulmonary bypass. Anesth Analg 1990;71:88–91. 10. Toyoyama H, Kariya N, Toyoda Y. Electrocardiographic artifacts during shoulder arthroscopy using a pressure-controlled irrigation pump. Anesth Analg 2000;90:856–7. 11. Marsh R. ECG artifact in the OR. Health Devices 1991;20: 140–141. 12. Kossman CE. Unipolar electrocardiography of Wilson: a half century later. Am Heart J 1985;110:901–4. 13. Kligfield P, Gettes LS, Bailey JJ, et al. Recommendations for the standardization and interpretation of the electrocardiogram. Part II: the electrocardiogram and its technology, a scientific statement from the American Heart Association Electrocardiography and Arrhythmias Committee, Council on Clinical Cardiology; the American College of Cardiology Foundation; and the Heart Rhythm Society endorsed by the International Society for Computerized Electrocardiology. J Am Coll Cardiol 2007;49:1109–27. 14. Frank E. Theoretic analysis of the influence of heart-dipole eccentricity on limb leads, Wilson central-terminal voltage and the frontal-plane vectocardiogram. Circ Res 1953;1:380–8. 15. Wehr G, Peters RJ, Khalife K, et al. A vector-based, 5-electrode, 12-lead monitoring ECG (EASI) is equivalent to conventional 12-lead ECG for diagnosis of acute coronary syndromes. J Electrocardiol 2006;39:22–28. 16. Chantad D, Krittayaphong R, Komoltri C. Derived 12-lead electrocardiogram in the assessment of ST-segment deviation and cardiac rhythm. J Electrocardiol 2006;39:7–12. 17. Sejersten M, Wagner GS, Pahlm O, et al. Detection of acute ischemia from the EASI-derived 12-lead electrocardiogram and from the 12-lead electrocardiogram acquired in clinical practice. J Electrocardiol 2007;40:120–6. 18. Welinder A, Field DQ, Liebman J, et al. Diagnostic conclusions from the EASI-derived 12-lead electrocardiogram as compared

19.

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33.

34.

35.

with the standard 12-lead electrocardiogram in children. Am Heart J 2006;151:1059–64. Dower GE, Yakush A, Nazzal SB, et al. Deriving the 12-lead electrocardiogram from four (EASI) electrodes. J Electrocardiol 1988:21 Suppl:S182–7. Sundqvist K, Jogestrand T, Nowak J. The effect of digoxin on the electrocardiogram of healthy middle-aged and elderly patients at rest and during exercise–a comparison with the ECG reaction induced by myocardial ischemia. J Electrocardiol 2002;35: 213–21. Mooss AN, Prevedel JA, Mohiuddin SM, et al. Effect of digoxin on ST-segment changes detected by ambulatory electrocardiographic monitotring in healthy subjects. Am J Cardiol 1991;68: 1503–6. Croft CH, Woodward W, Nicod P, et al. Clinical implications of anterior S–T segment depression in patients with acute myocardial infarction. Am J Cardiol 1982;50:428–36. Mirvis DM. Physiologic bases for anterior ST segment depression in patients with acute inferior wall myocardial infarction. Am Heart J 1988;116:1308–22. Rahman MA, Gedevanishvili A, Birnbaum Y, et al. High-frequency QRS electrocardiogram predicts perfusion defects during myocardial perfusion imaging. J Electrocardiol 2006;39:73–81. Abboud S, Berenfeld O, Sadeh D. Simulation of high-resolution QRS complex using a ventricular model with a fractal conduction system. Effects of ischemia on high-frequency QRS potentials. Circ Res 1991;68:1751–60. Pettersson J, Carro E, Edenbrandt L, et al. Spatial, individual, and temporal variation of the high-frequency QRS amplitudes in the 12-lead standard electrocardiographic leads. Am Heart J 2000;139:352–8. Aversano T, Rudicoff B, Washington A, et al. High-frequency QRS electrocardiography in the detection of reperfusion following thrombolytic therapy. Clin Cardiol 1994;17:175–82. Pettersson J, Pahlm O, Carro E, et al. Changes in high-frequency QRS components are more sensitive than ST-segment deviation for detecting acute coronary artery occlusion. J Am Coll Cardiol 2000;36:1827–34. Spackman TN, Abel MD, Schlegel TT. Twelve-lead high frequency QRS electrocardiography during anesthesia in healthy subjects. Anesth Analg 2005;100:1043–7. Lindenauer PK, Pekow P, Wang K, et al. Perioperative beta-blocker therapy and mortality after major noncardiac surgery. N Engl J Med 2005;353:349–361. Mangano DT, Browner WS, Hollenberg M, et al. Association of perioperative myocardial ischemia with cardiac morbidity and mortality in men undergoing noncardiac surgery. The Study of Perioperative Ischemia Research Group. N Engl J Med 1990;323:1781–8. London MJ. Perioperative myocardial ischemia in patients undergoing myocardial revascularization. Curr Opin Anesthesiol 1993;6:98–105. McFalls EO, Ward HB, Moritz TE, et al. Predictors and outcomes of a perioperative myocardial infarction following elective vascular surgery in patients with documented coronary artery disease: results of the CARP trial. Eur Heart J 2008;29:394–401. Karpati PC, Rossignol M, Pirot M, et al. High incidence of myocardial ischemia during postpartum hemorrhage. Anesthesiology 2004;100:30–36. Blackburn H, Katigbak R. What electrocardiographic leads to take after exercise? Am Heart J 1964;67:184–5.

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36. Mason RE, Likar I. A new system of multiple-lead exercise electrocardiography. Am Heart J 1966;71:196– 205. 37. Mason RE, Likar I, Biern RO, et al. Multiple-lead exercise electrocardiography: Experience in 107 normal subjects and 67 patients with angina pectoris, and comparison with coronary cinearteriography in 84 patients. Circulation 1967;36: 517–25. 38. Tubau JF, Chaitman BR, Bourassa MG, et al. Detection of multivessel coronary disease after myocardial infarction using exercise stress testing and multiple ECG lead systems. Circulation 1980;61:44–52. 39. Koppes G, McKiernan T, Bassan M, et al. Treadmill exercise testing (part I). Curr Prob Cardiol 1977;7:1–44. 40. Chaitman BR, Bourassa MG, Wagniart P, et al. Improved efficiency of treadmill exercise testing using a multiple-lead ECG system and basic hemodynamic exercise response. Circulation 1978;57:71–79. 41. Miller TD, Desser KB, Lawson M. How many electrocardiographic leads are required for exercise treadmill tests? J Electrocardiol 1987;20:131–7. 42. Lam J, Chaitman BR. Exercise lead systems and newer electrocardiographic parameters. J Cardiac Rehabil 1984;4:507–16. 43. Chaitman BR. The changing role of the exercise electrocardiogram as a diagnostic and prognostic test for chronic ischemic heart disease. J Am Coll Cardiol 1986;8:1195– 1210. 44. Chaitman BR, Hanson JS. Comparative sensitivity and specificity of exercise electrocardiographic lead systems. Am J Cardiol 1981;47:1335–49.

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45. Horacek BM, Wagner GS. Electrocardiographic ST-segment changes during acute myocardial ischemia. Card Electrophysiol Rev 2002;6:196–203. 46. Carley SD. Beyond the 12 lead: review of the use of additional leads for the early electrocardiographic diagnosis of acute myocardial infarction. Emerg Med (Fremantle) 2003;15:143–54. 47. Drew BJ, Krucoff MW. Multilead ST-segment monitoring in patients with acute coronary syndromes: a consensus statement for healthcare professionals. ST- Segment Monitoring Practice Guideline International Working Group. Am J Crit Care 1999;8:372–86. 48. London MJ, Hollenberg M, Wong MG, et al. Intraoperative myocardial ischemia: localization by continuous 12-lead electrocardiography. Anesthesiology 1988;69:232–41. 49. Landesberg G, Mosseri M, Wolf Y, et al. Perioperative myocardial ischemia and infarction: identification by continuous 12-lead electrocardiogram with online ST-segment monitoring. Anesthesiology 2002;96:264–70. 50. Drew BJ, Krucoff MW. Multilead ST-segment monitoring in patients with acute coronary syndromes: a consensus statement for healthcare professionals. ST- Segment Monitoring Practice Guideline International Working Group. Am J Crit Care 1999;8:372–86. 51. London MJ. Multilead precordial ST-segment monitoring: “the next generation”? Anesthesiology 2002;96:259–61. 52. Martinez EA, Kim LJ, Faraday N, et al. Sensitivity of routine intensive care unit surveillance for detecting myocardial ischemia. Crit Care Med 2003;31:2302–8. 53. Balaji S, Ellenby M, McNames J, et al. Update on intensive care ECG and cardiac event monitoring. Card Electrophysiol Rev 2002;6:190–5.

Chapter

6

Arterial pressure monitoring Alexander J. C. Mittnacht and Tuula S. O. Kurki

Introduction Blood pressure (BP) is the one of the most commonly measured parameters of the cardiovascular system. The American Society of Anesthesiologists (ASA) guidelines for basic anesthesia monitoring, available online at http://www.asahq. org/publicationsAndServices/standards/02.pdf (last amended October 2005), mandate that arterial blood pressure be determined and evaluated at least every five minutes. Numerous methods of noninvasive BP measurement, next to the invasive assessment via an indwelling catheter, are clinically available.1,2 Technical concepts, evidence of utility, indications, contraindications, and complications of blood pressure monitoring are discussed in this chapter.

Technical concept General principles Arterial BP, typically recorded as a systolic, diastolic, and mean arterial pressure (MAP) in millimeters of mercury, is derived from the complex interaction of the heart and the vascular system and varies not only at different sites in the body, but also when individual components of this system are changed. Stroke volume, systemic vascular resistance, the velocity of left ventricular ejection, the distensibility of the aorta and arterial walls, and the viscosity of blood all are components of this complex interaction that ultimately results in a pressure reading. The arterial BP can also be seen as the force exerted by the blood per unit area on the arterial wall, with kinetic, hydrostatic, and hemodynamic individual pressure components contributing. After an arterial catheter has been placed, the typical arterial waveform can be displayed and recorded. However, this waveform actually represents the summation of a series of mechanical pressure signals or waves (multiple harmonics). The sine wave occurring at the rate of the pulse is called the fundamental frequency; each subsequent harmonic is a multiple of this first harmonic. Six to ten of those subsequent harmonics are required to reconstruct and to display the arterial pressure waveform (see Figure 6.1).3,4 The components of the monitoring system – the cannula, tubing, connectors, and pressure transducer – all have their own natural resonant frequencies. Accurate pressure readings can be obtained only if the natural frequency of the monitoring system does not overlap with

harmonic frequencies of the recorded pressure waveforms (also see invasive BP monitoring, discussed later).

Noninvasive BP measurement Numerous methods of noninvasive BP measurement are clinically available. The American Heart Association (AHA) has published updated recommendations for noninvasive blood pressure measurements in humans.5,6 The traditional auscultatory method is still considered the gold standard against which all other devices and methods must be compared. Using a stethoscope and a sphygmomanometer with an inflatable cuff placed around the upper arm, one can determine the systolic and diastolic BP. The height of a mercury (Hg) column in millimeters at the auscultatory determined systolic and diastolic points is reported. The systolic BP is the pressure at which the first sound is heard; the exact diastolic BP is more difficult to determine. The use of the fifth Korotkoff sound for diastolic BP measurement is typically used; however, the fourth Korotkoff sound has been recommended in certain clinical situations.6 Appropriate cuff size is mandatory, as too small a cuff will yield false high, and too large a cuff false low, BP values. Even though a mercury sphygmomanometer does not need repeated calibration, accurate results are operator-dependent (observer error), and limitations of this method in various clinical settings must be recognized.6 Automated BP devices have replaced the auscultatory method in most anesthesia practice settings. Most of these devices use a cuff that is inflated by an electrically operated pump. A pressure release valve regulates the pressure in the cuff, with different manufacturers using various algorithms and intervals. All devices display systolic, diastolic, and mean arterial blood pressure and a pulse rate. However, it is important to recognize that typically only the mean arterial BP is determined or measured by oscillatory BP devices; the values of systolic and diastolic BP are computed, not actually measured, from the raw data. Similar to the auscultatory method, the appropriate cuff size is important for determining exact BP values. Available devices and the various methods used vary widely in accuracy; devices should be checked and, if necessary, recalibrated by qualified personal at specified intervals. The US Association for the Advancement of Medical Instrumentation (AAMI) and the British Hypertension Society (BHS) have set standards and

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Fundamental Wave

P-cuff P-arterial

Harmonic Wave

Cuff

Summation Wave Figure 6.1. The arterial pressure waveform as a sum of sine waves by Fourier analysis. Summation of the top and middle sine waves produces a waveform with the morphologic characteristics of an arterial blood pressure trace. From Pittman JAL, Ping JS, Mark JB. Arterial and central venous pressure monitoring. Anesthesiol Clin 2006;24:717–35 (Figure 1), with permission.

protocols for the evaluation of blood pressure device accuracy.7–9 The Working Group on Blood Pressure Monitoring of the European Society of Hypertension reviews blood pressure measuring devices to guide consumers. There are many sources of inaccurate pressure measurements with automated oscillatory methods, such as irregular heart rate seen with arrhythmias, low flow states, arm movement during BP measurement, and inappropriate positioning of the measurement site or cuff in relation to the heart. Continuous beat-to-beat BP monitoring with noninvasive devices has been reported.10,11 The volume-clamp method, tonometry, and photoplethysmographic methods have been described. The volume-clamp method was first described by Jan Pe˜na´z in 1973.12 The criterion to determine the correct unloaded volume by applying a physiologic calibration (Physiocal) was developed by Wesseling and colleagues.13 The combination of these methods allows the continuous beat-to-beat BP measurement with a finger cuff placed on a patient’s finger (FINAP). Commercially available devices consist of a finger cuff that contains the transducer of an infrared transmission plethysmograph (also see Figures 6.2 and 6.3). Infrared light is absorbed by the blood, and the pulsation of arterial diameter during a heartbeat causes a pulsation in the light detector signal. The cuff is wrapped around the middle phalanx of a finger (index or middle finger is recommended) and is connected to a pressure control valve. This proportional valve modulates the air pressure generated by the air compressor, thus causing changes in the finger cuff pressure in parallel with intraarterial pressure in the finger to dynamically unload the arterial walls in the finger. The cuff pressure thus provides an indirect measure of intraarterial pressure. In addition to continuous arterial BP monitoring, further developments of this technique allow computation of stroke volume, cardiac output, pulse rate variability, baroreflex sensitivity, total peripheral resistance, and systolic pressure variability.14 The accuracy of the FINAP has been tested in several clinical trials against oscillometric blood

46

Bone

Arteries

IR LED

Finger

Photo diode

Plethysmogram Figure 6.2. Cross-section of a finger at the middle phalanx level with a finger cuff wrapped around on it with built-in infrared (IR) plethysmograph. Source: Nexfin device, BMEYE, Amsterdam, The Netherlands.

pressure measurement, or noninvasive blood pressure (NIBP), and against invasive intraarterial pressure measurement.15 The FINAP seems to underestimate the invasive systolic blood pressure (SBP). Raynaud syndrome, anatomical variations in palmar arch arterial circulation, and the use of vasoconstricting agents are some of the factors that, if present, may yield inaccurate BP readings using the FINAP method.16,17 The underor overestimation of systolic pressure by changes in vasomotor tone has been mostly corrected for by reconstructing the brachial blood pressure waveform from the measured finger arterial pressure.18,19 This brachial reconstruction has been validated in a new device based on the integration of these technologies.20

Invasive arterial blood pressure monitoring Pressure waves in the arterial (or venous) tree represent the transmission of forces generated in the cardiac chambers. Measurement of these forces requires their transmission to a device that converts mechanical energy into electronic signals. The components of a system for intravascular pressure measurement include an intravascular catheter, fluid-filled tubing and connections, an electromechanical transducer, an electronic analyzer, and electronic storage and display systems.

Arterial cannulation For arterial pressure measurements, short, narrow catheters (20-gauge or smaller) are recommended, because they have favorable dynamic response characteristics and are less thrombogenic than larger catheters. An artifact associated with intraarterial catheters has been labeled end-pressure artifact.21 When flowing blood comes to a sudden halt at the tip of the

Chapter 6 – Arterial Pressure Monitoring

A

B Figure 6.3. Arterial pressure registration (with Nexfin device; BMEYE, Amsterdam, The Netherlands) – nitroglycerin response Top (A): noninvasive–brachial arterial pressure [0-200 mmHG; (B) invasive–radial A-line pressure 0-200 mmHg. Horizontal = time [sec], time in measurement. Patient – female, 62 yrs, supine CABG surgery, anesthetized. Source: JJ Settels, BMEYE, Amsterdam, The Netherlands

catheter, it is estimated that an added pressure of 2 to 10 mmHg results. Conversely, clot formation on the catheter tip will overdamp the system (as discussed later). Proper technique is helpful in obtaining a high degree of success in arterial catheterization. The wrist should be placed in a slightly dorsiflexed position, preferably over an armboard and over a pack of gauze in a supinated position. Caution should be exercised not to keep the wrist in extreme dorsiflexion, which can lead to median nerve damage by stretching of the nerve over the wrist. The angle between the needle and the skin should be shallow (30 degrees or less), and the needle should be advanced parallel to the course of the artery. When the artery is entered, the angle between the needle and skin is reduced to 10 degrees, the needle is advanced another 1 to 2 mm to ensure that the tip of the catheter also lies within the lumen of the vessel, and the outer catheter is then threaded off the needle whilewatching that blood continues to flow out of the needle hub. If blood ceases flowing while the needle is being advanced, the needle has penetrated the back wall of the vessel. In this technique, the artery has been transfixed by passage of the catheter-overneedle assembly “through-and-through” the artery. The needle is then completely withdrawn. As the catheter is slowly

withdrawn, pulsatile blood flow emerges from the catheter when its tip is within the lumen of the artery. The catheter is then slowly advanced into the artery. A guidewire may be helpful at this point if the catheter does not advance easily into the artery. When using the Seldinger technique, the artery is localized with a needle, and a guidewire is passed through the needle into the artery. A catheter is then passed over the guidewire into the artery. Doppler-assisted localization of arteries has been used when palpation of the artery is difficult. However, Doppler-assisted techniques have been largely supplanted in clinical practice by two-dimensional ultrasonic methods. In the case of arterial catheterization, especially radial artery cannulation, a highfrequency (e.g. 9 MHz) ultrasonic transducer is required to visualize small structures in the near field. The artery is visualized in transverse section and the catheter-over-needle assembly is advanced at a 30- to 60-degree angle, starting a few millimeters distal to the ultrasonic transducer. With experience, the artery and the catheter are seen to intersect within the ultrasonic imaging plane using a triangulation technique. Alternatively, viewing the artery in a longitudinal imaging plane during needle insertion has been described. Using a two-dimensional

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ultrasound imaging technique for radial artery cannulation has been shown to increase the success rate at first attempt.22 Nevertheless, there seems to be a significant learning curve involved. Following the introduction of two-dimensional ultrasonic vascular access devices, a surgical cutdown as the last resort is typically performed less frequently. For a surgical cutdown technique, an incision is made in the skin overlying the artery, and the surrounding tissues are dissected away from the arterial wall. Proximal and distal ligatures are passed around the artery to control blood loss, but are not tied down. Under direct vision, the artery is cannulated with a catheter-over-needle assembly. Alternatively, a small incision is made in the arterial wall to facilitate passage of the catheter.

Arterial cannulation sites Factors that influence the site of arterial cannulation include the location of surgery, the possible compromise of arterial flow owing to patient positioning or surgical manipulations, and any history of ischemia of or prior surgery on the limb to be cannulated. Sites for arterial cannulation include the radial, ulnar, brachial, axillary, femoral, and dorsalis pedis or posterior tibial arteries. The radial artery is the most commonly used artery for continuous invasive BP monitoring. It is usually easy to cannulate with a short (20-gauge) catheter and is readily accessible during surgery. The predictive value of testing adequate palmar collateral circulation with the Allen test has been questioned. The Allen test is performed by compressing both the radial and ulnar arteries and exercising the hand until it is pale. The ulnar artery is then released (with the hand open loosely), and the time until the hand regains its normal color is noted.23 With normal collateral circulation, the color returns to the hand in about five seconds. If, however, the hand takes longer than 15 seconds to return to its normal color, cannulation of the radial artery on that side is controversial. In a large series of children in whom radial arterial catheterization was performed without preliminary Allen tests, there was an absence of complications.24 Slogoff and coworkers cannulated the radial artery in 16 adult patients with poor ulnar collateral circulation (assessed using the Allen test) without any complications.25 An incidence of zero in a study sample of only 16 patients, however, does not guarantee that the true incidence of the complication is negligible. In contrast, Mangano and Hickey reported a case of hand ischemia requiring amputation in a patient with a normal preoperative Allen test.26 Alternatively, pulse oximetry or plethysmography can be used to assess patency of the hand collateral arteries. Barbeau and associates compared the modified Allen test with pulse oximetry and plethysmography in 1010 consecutive patients undergoing percutaneous radial cannulation for cardiac catheterization.27 Pulse oximetry and plethysmography were more sensitive than the Allen test for detecting inadequate collateral blood supply, and only 1.5 percent of patients were not suitable for radial artery cannulation.

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Brachial artery cannulation is routinely performed at many institutions, although others question the safety of this technique, given the fact that there is little, if any, collateral flow to the hand should brachial artery occlusion occur. Brachial artery pressure tracings resemble those in the femoral artery, with less systolic augmentation than radial artery tracings.28 Brachial arterial pressures were found to more accurately reflect central aortic pressures than radial arterial pressures, both before and after cardiopulmonary bypass.29 The axillary artery is normally cannulated using the Seldinger technique near the junction of the deltoid and pectoral muscles. This approach has been recommended for longterm catheterization in the intensive care unit and in patients with peripheral vascular disease.30 Because the tip of the 15to 20-cm catheter may lie within the aortic arch, the use of the left axillary artery is recommended to minimize the theoretical risk of cerebral embolization during flushing. Lateral decubitus positioning or adduction of the arm occasionally results in kinking of axillary catheters with damping of the pressure waveform. The femoral artery may be cannulated for monitoring purposes but is usually reserved for situations when other sites are unable to be cannulated or it is specifically indicated (e.g. descending thoracic aortic aneurysm surgery for distal pressure monitoring). The use of this site remains controversial because of the risk of ischemic complications and pseudoaneurysm formation following diagnostic angiographic and cardiac catheterization procedures. However, these data do not pertain to the clinical situation when the femoral artery is used for monitoring purposes, because the size of catheters for BP monitoring is considerably smaller than the size of diagnostic catheters. A literature review on peripheral artery cannulation placed for hemodynamic monitoring purposes (including 3899 femoral artery cannulations) found temporary occlusion in 10 patients (1.45%), whereas serious ischemic complications requiring extremity amputation were reported in only three patients (0.18%).31 Other complications that were summarized from the published data were pseudoaneurysm formation in six patients (0.3%), sepsis in 13 patients (0.44%), local infection (0.78%), bleeding (1.58%), and hematoma (6.1%). The researchers concluded that, based on the reviewed literature, using the femoral artery for hemodynamic monitoring purposes was safer than radial artery cannulation. Older literature stated that the femoral area was intrinsically dirty, and that catheter sepsis and mortality were significantly increased at this site compared with other monitoring sites. This could also not be confirmed by more recently published literature.32 The two main arteries to the foot are the dorsalis pedis artery and the posterior tibial artery, which form an arterial arch on the foot that is similar to the one formed by the radial and ulnar arteries in the hand. The dorsalis pedis or posterior tibial arteries are reasonable alternatives to radial arterial catheterization. The systolic pressure is usually 10 to 20 mmHg higher in the dorsalis pedis artery than in the radial or brachial arteries, whereas the diastolic pressure is 15 to 20 mmHg lower.33

Chapter 6 – Arterial Pressure Monitoring

Aortic Root Subclavian Axillary

Brachial

Radial Femoral Dorsalis Pedis

Figure 6.4. The waveform of the arterial pressure changes markedly according to the site of the intraarterial catheter. This illustration demonstrates these changes as a progression from central monitoring (top) through peripheral monitoring (bottom). These changes are believed to be caused by forward wave propagation and wave reflection. In the periphery, systolic pressure is higher, diastolic pressure is lower, and mean pressure is minimally lower. Modified from Bedford RF. Invasive blood pressure monitoring. In Blitt CD (ed.). Monitoring in Anesthesia and Critical Care. New York: Churchill Livingstone, 1985, p. 505.

The incidence of failed cannulation is up to 20 percent, and the incidence of thrombotic occlusion is around 8 percent, because of the small size of the artery.34 In a recently published prospective observational study, dorsalis pedis artery cannulation was found to be a safe and easily available alternative when radial arteries are not accessible.35 However, these vessels should not be used in patients with severe peripheral vascular disease from diabetes mellitus or other causes.

Arterial pressure waveform The arterial pressure waveform is ideally measured in the ascending aorta. The pressure measured in the more peripheral arteries is different from the central aortic pressure because the arterial waveform becomes progressively more distorted as the signal is transmitted down the arterial system. The highfrequency components, such as the dicrotic notch, disappear; the systolic peak increases; the diastolic trough decreases; and there is a transmission delay (distal pulse amplification; see Figure 6.4). These changes are caused by decreased arterial compliance in the periphery, and reflection and resonance of pressure waves in the arterial tree.36 This effect is most pronounced in the dorsalis pedis artery, in which the SBP may be 10 to 20 mmHg higher, and the diastolic blood pressure (DBP) 10 to 20 mmHg lower than in the central aorta. Despite this distortion, the MAP measured in the peripheral arteries should be similar to the central aortic pressure under normal circumstances. Thus, the cannulation of large more central arterial

vessels, such as the femoral and axillary arteries, can be avoided in most clinical settings.37 MAP is probably the most useful parameter to measure in assessing organ perfusion, except for the heart, in which the DBP is the most important. MAP is measured directly by integrating the arterial waveform tracing over time, or using the formula: MAP = (SBP + [2 × DBP])/3. The pulse pressure is the difference between SBP and DBP. Arterial waveform analysis – and, in particular, the influence of positive pressure ventilation on the cyclic variation of the arterial pressure – has been studied.38–40 The interactions among intrathoracic pressure, lung volume, and left- and rightsided loading conditions are complex, and cannot be easily interpreted. Typically, increased variation in arterial pressure is seen in hypovolemic patients, and its response to fluid administration has been studied in animals and humans. Systolic pressure variation (SPV) is typically described as the increase (⌬ up) and decrease (⌬ down) from end-expiratory baseline during positive pressure ventilation (see Figure 6.5). In particular, ⌬ down has been shown to be a sensitive marker for hypovolemia. However, tidal volume, airway pressures, lung and chest wall compliance, positive end-expiratory pressure, and arrhythmias all have been shown to interfere with the magnitude of SPV and its components.

Coupling system and pressure transducers The coupling system usually consists of pressure tubing, stopcocks, and a continuous flushing device. This fluid-filled system, once attached to the arterial cannula, oscillates in its own inherent frequency. This is called resonance and is the major source of distortion of arterial pressure tracings. The function of transducers is to convert mechanical forces into electrical current or voltage. Modern disposable transducers have eliminated many of the difficulties that formerly required frequent recalibration owing to zero-point drift. Before accurate pressure values can be obtained, transducers must be zeroed against ambient atmospheric pressure and horizontally aligned (leveled) with the right atrium. In fluid-filled catheter systems, incorrect positioning of the transducer can be a major source of inaccurate pressure readings. This is of particular concern in the low-pressure venous system, because small changes in transducer height will have a proportionally large effect on the pressure readings. If cerebral perfusion is of interest – for example, during intracranial procedures in the sitting position – the pressure transducer should be placed at the level of the circle of Willis rather than the right atrium. Calibration of modern transducers is done by the manufacturer and is thus not required in the clinical setting. Most modern equipment designed to analyze and display pressure information consists of a computerized system that handles several tasks, including the acquisition and display of pressure signals; the derivation of numerical values for systolic, diastolic, and mean pressures; alarm functions; data storage; trend displays; and printing functions. When connected to an

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Monitoring in Anesthesia and Perioperative Care

SPmax SPnet SPmin

Δ up

Pa

Paw

SPV

Δ down

Figure 6.5. Analytic description of respiratory changes in arterial pressure during mechanical ventilation. The systolic pressure and the pulse pressure (systolic minus diastolic pressure) are maximum (SPmax and PPmax , respectively) during inspiration and minimum (SPmin and PPmin , respectively) a few heartbeats later – i.e. during the expiratory period. The systolic pressure variation (SPV) is the difference between SP max and SPmin . The assessment of a reference systolic pressure (SPref ) during an end-expiratory pause allows the discrimination between the inspiratory increase (⌬ up) and the expiratory decrease (⌬ down) in systolic pressure. Pa = arterial pressure; Paw = airway pressure. From reference 40.

End-expiratory pause ΔPP = 100 × (PPmax − PPmin)/[(PPmax + PPmin)/2] Pa

PPmax PPmin

automated anesthesia recordkeeping system, BP readings can be recorded automatically and linked to various perioperative measured parameters and events.

Characteristics of a pressure measurement system The dynamic response of a pressure measurement system is characterized by its natural frequency and its damping.41 These concepts are best understood by snapping the end of a transducer–tubing assembly with one’s finger. The waveform on the monitor demonstrates rapid oscillations above and below

Figure 6.6. The arterial pressure artifact resulting from a fast flush test allows calculation of the natural resonant frequency and the damping coefficient of the monitoring system. The time between adjacent pressure peaks determines the natural frequency and the height or amplitude ratio of adjacent peaks allows determination of the damping coefficient. From reference 27.

50

the baseline, which is equal to the natural frequency, and then quickly decays to a straight line because of friction in the system (damping; also see Figures 6.6 and 6.7). The peaks and troughs of an arterial pressure waveform will be amplified, resulting in inaccurate pressure readings if the natural frequency of the transducer–tubing–catheter assembly is too low. The natural frequency of the measurement system needs to be at least six to 10 times higher than the fundamental frequency of the pressure wave (heart rate). Consequently, with a heart rate of 120 beats per minute (2 cycles per second or 2 Hz), a natural frequency ⬎ 20 Hz of the monitoring system is required to accurately display the arterial pressure.42 Boutros and Albert demonstrated that by changing the length of low-compliance (rigid) tubing from 6 inches to 5 feet, the natural frequency decreased from 34 to 7 Hz.43 As a result of the reduced natural frequency, the SBPs measured with the longer tubing exceeded reference pressures by 17.3 percent. Generally, longer transducer tubing lowers the natural frequency of the system and tends to amplify the height of the systolic (peak) and the depth of the diastolic (trough) values of the BP measurement.44,45 Damping is the tendency of factors such as friction, compliant (soft) tubing, and air bubbles to absorb energy and decrease the amplitude of peaks and troughs in the waveform. The optimal degree of damping is that which counterbalances the distorting effects of transducer–tubing systems with lower natural frequencies. This is very difficult to achieve. The damping of a clinical pressure measurement system can be assessed by observing the response to a rapid high-pressure flush of the transducer–tubing–catheter system (also see Figures 6.6 and 6.7). In a system with a low damping coefficient, a fast flush test will result in several oscillations above and below the baseline before the pressure becomes constant. In an adequately damped system, the baseline will be reached after one

Chapter 6 – Arterial Pressure Monitoring

100

A

0 200

100

B

120/54 MP = 01

0 200

Figure 6.7. The fast flush test demonstrates the harmonic characteristics of a pressure monitoring system (transducer, fluid-filled tubing, and intraarterial catheter). In an optimally damped system (A), the pressure waveform returns to baseline after only one oscillation. In an underdamped system (B), the pressure waveform oscillates above and below the baseline several times. In an overdamped system (C), the pressure waveform returns to the baseline slowly with no oscillations. Modified from reference 49.

100

C

0

oscillation, whereas in an overdamped system, the baseline will be reached after a delay and without oscillations.46–49 The formulas for calculating the natural frequency and damping coefficient are as follows:  3 d Natural frequency : f n = 8 ␲L␳Vd  16n Damping coefficient : ␨ = 3 d

3LVd , ␲␳

where d = tubing diameter; L = tubing length; ␳ = density of the fluid; Vd = transducer fluid volume displacement; and n = viscosity of the fluid.

Evidence of utility (clinical outcome) Multiple well-designed prospective studies have established the correlation between elevated BP and cardiovascular events. These data are well presented in the literature and are beyond the scope of this text.50 Intraoperative measurement of BP is required by the ASA (as mentioned earlier), and outcome studies comparing the use of this parameter to a nonmonitored group are not feasible. However, there is increasing evidence that an increase in perioperative BP, as well as pulse pressure (PP), are associated with adverse events and outcome measures in cardiac as well as noncardiac surgical settings.51 Fontes and colleagues recently published on the association between an increased PP and

adverse cerebral and cardiac events.52 A total of 4801 patients scheduled for elective coronary bypass surgery met the inclusion criteria. Nine hundred seventeen patients (19.1%) had fatal and nonfatal vascular complications, including 146 patients (3.0%) with cerebral events and 715 patients (14.9%) with cardiac events. The incidence of a cerebral event and/or death from neurologic complications nearly doubled for patients with PP ⬎80 mmHg versus PP ≤ 80 mmHg (5.5% vs. 2.8%; P = 0.004). PP more than 80 mmHg was also found to be associated with cardiac complications, increasing the incidence of congestive heart failure by 52 percent, and death from cardiac causes by nearly 100 percent (P = 0.003 and 0.006, respectively). The same group reported in an earlier study that isolated systolic hypertension is associated with increased cardiovascular morbidity in coronary artery surgery patients.53 In another large prospective observational study, 7740 noncardiac surgery cases (general, vascular, and urological surgery) were included in the analysis. Intraoperative arterial hypertension was an independent predictor of cardiac adverse events within 30 days of surgery (83 patients, 1.1%).54

Complications The complications of percutaneous arterial cannulation are summarized in Table 6.1. Despite the great advantages of intraarterial monitoring, it does not always give accurate BP values. Equipment misuse and misinterpretation have been reported as the most frequent complications associated with invasive pressure monitoring.55 The monitoring system may be incorrectly zeroed and calibrated, or the transducers may not be at the appropriate level. The waveform will be dampened if the catheter is kinked or partially thrombosed. In vasoconstricted patients, in patients in hypovolemic shock, and during the post-CPB period, the brachial and radial artery pressures may be significantly lower than the true central aortic pressure. With modern transducers, baseline drift has become less frequent; however, fluid contamination of transducer cable connectors or faulty transducer cables can give inaccurate readings. Another possible etiology for inaccurate measurements is unsuspected arterial stenosis proximal to the monitored artery, as occurs with thoracic outlet syndrome and subclavian stenosis. One potential complication that is common to all forms of invasive monitoring is infection. Indwelling percutaneous catheters can become infected because of insertion through an Table 6.1. • • • • • • • •

Complications of invasive arterial pressure monitoring

False pressure readings (equipment misuse) Infection Bleeding, hematoma formation Thrombosis Ischemia Cerebral emboli Nerve damage Pseudoaneurysm

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Monitoring in Anesthesia and Perioperative Care

infected skin site, poor aseptic technique during insertion or maintenance, sepsis with seeding of the catheter, and prolonged duration of cannulation with colonization by skin flora.56 Historically, factors that were associated with catheter infection included nondisposable transducer domes, dextrose flush solutions, contaminated blood gas syringes, and duration of insertion.57–60 Recently published data suggest that the incidence of arterial catheter infection is similar to infection rates published with the insertion of central venous catheters.61,62 However, in contrast with central venous catheterization, full sterile barriers during arterial line placement were not found to reduce the risk of arterial catheter infections.63,64 Nevertheless, these data do not exempt the practitioner from using strict aseptic techniques. Guidelines for the prevention of intravascular catheter related infections have been published by the Hospital Infection Control Practices Advisory Committee and the Centers for Disease Control and Prevention.65 The use of an intraarterial catheter carries the potential risk of exsanguination if the catheter or tubing assembly becomes disconnected. The use of Luer-Lok (instead of tapered) connections and monitors with low-pressure alarms should decrease the risk of this complication. Stopcocks are an additional source of occult hemorrhage because of the potential for loose connections or inadvertent changes in the position of the control lever that would open the system to the atmosphere. Thrombosis of the radial artery following cannulation has been studied extensively. Temporary arterial occlusion is the most common reported complication after radial artery cannulation.66 Factors that correlate with an increased incidence of thrombosis include prolonged duration of cannulation,67 larger catheters,68 and smaller radial artery size (i.e. a greater proportion of the artery is occupied by the catheter).69 The association between radial artery thrombosis and ischemia of the hand is less certain. As noted above, an abnormal Allen test was not associated with hand complications following radial artery cannulation.25 Despite the widespread use of radial artery cannulation, hand complications are very rarely reported. Temporary occlusion after arterial cannulation is usually benign. Nevertheless, serious ischemic complications are reported that may require the amputation of a digit or extremity.70–72 Slogoff and associates stated that, in their experience, most ischemic complications occurred in patients who had had multiple embolic phenomena from other sources or were on highdose vasopressor therapy, with resultant ischemia in multiple extremities.25 The hand should be examined closely at regular intervals in patients with axillary, brachial, radial, or ulnar arterial catheters. Because thrombosis may appear several days after the catheter has been removed,67 the examinations should be continued through the postoperative period. Although recanalization of the thrombosed artery can be expected in an average of 13 days,73 the collateral blood flow may be inadequate during this period. The treatment plan should involve consultation

52

with a vascular, hand, or plastic surgeon. Traditionally, treatment for arterial occlusion or thrombosis with adequate collateral flow has been conservative. However, fibrinolytic agents, such as streptokinase, stellate ganglion blockade, and/or surgical intervention are modalities that should be considered. Overall, the evidence of permanent hand ischemia is low. Particulate matter or air that is flushed forcefully into an arterial catheter can move proximally as well as distally within the artery. Cerebral embolization is most likely from axillary or temporal sites, but is also possible with brachial and radial catheters.74 Emboli from the right arm are more likely to reach the cerebral circulation than those from the left arm because of the anatomy and direction of blood flow in the aortic arch. Other factors that influence the likelihood of cerebral embolization include the volume of flush solution, the rapidity of the injection, and the proximity of the intraluminal end of the catheter to the central circulation.75 Hematoma formation may occur at any arterial puncture or cannulation site, and is particularly common with a coagulopathy. Hematoma formation should be prevented by the application of direct pressure following arterial punctures and, if possible, the correction of any underlying coagulopathy. Posterior puncture or tear of the femoral or iliac arteries can produce massive bleeding into the retroperitoneal area.76 Surgical consultation should be obtained if massive hematoma formation develops. Nerve damage is possible if the nerve and artery lie in a fibrous sheath (such as the brachial plexus) or in a limited tissue compartment (such as the forearm).77 Direct nerve injuries may also occur from needle trauma during attempts at arterial cannulation. The median nerve is in close proximity to the brachial artery, and the axillary artery lies within the brachial plexus sheath. Incomplete disruption of the wall of an artery may eventually result in pseudoaneurysm formation.78 The wall of the pseudoaneurysm is composed of fibrous tissue that continues to expand. If the pseudoaneurysm ruptures into a vein, or if both a vein and an artery are injured simultaneously, an arteriovenous fistula may result. Nonsurgical treatment options for the repair of pseudoaneurysms after arterial cannulation have been described recently and may replace surgery that is usually performed to treat this complication.79

Credentialing The AHA recommendations for blood pressure measurements in humans, available online at http://circ.ahajournals. org/cgi/content/full/111/5/697 (last amended 2005), list recommendations for observer training. The training should be the same for health care professionals in ambulatory and community settings, as well as lay observers. Required competencies such as adequate vision, hearing, and eye–hand–ear coordination should be assessed prior to training. Actual training

Chapter 6 – Arterial Pressure Monitoring

Table 6.2. • • • • • • • • • • • • •

Indications for invasive arterial pressure monitoring

Major surgical procedures involving large fluid shifts and/or blood loss Surgery requiring cardiopulmonary bypass Surgery of the aorta Patients with pulmonary disease requiring frequent arterial blood gases Patients with recent myocardial infarctions, unstable angina, or severe coronary artery disease Patients with decreased left ventricular function (congestive heart failure) or significant valvular heart disease Patients in hypovolemic, cardiogenic, or septic shock, or with multiple organ failure Procedures involving the use of deliberate hypotension Massive trauma cases Patients with right heart failure, chronic obstructive pulmonary disease, pulmonary hypertension, or pulmonary embolism Hemodynamic instable patients requiring vasoconstrictive or inotropic pharmacological support Patients with electrolyte or metabolic disturbances requiring frequent blood samples Inability to measure arterial pressure noninvasively (e.g. morbid obesity)

can be provided in various settings; for clinical trials, however, standardized programs are recommended. For federally funded clinical trials of hypertension care and control, retraining is required every six months. Because the use of automated BP devices does not eliminate all sources of human error, training of observers is also recommended when automated devices are used.

Practice parameters (indications for arterial BP monitoring) The ASA guidelines for basic anesthesia monitoring mandate that arterial blood pressure be determined and evaluated at least every five minutes during all anesthetic procedures. There are no specific recommendations as to what procedures or clinical settings require invasive arterial blood pressure monitoring. Some of the typical indications for invasive arterial monitoring are listed in Table 6.2. Intraarterial monitoring provides a continuous, beat-to-beat indication of the arterial pressure and waveform, and having an indwelling arterial catheter enables frequent sampling of arterial blood for laboratory analyses. Thus, even with the ability to measure beat-tobeat BP noninvasively, direct intraarterial monitoring remains the gold standard for cases in which hemodynamic changes occur frequently and large fluid shifts are anticipated. Additionally, the arterial waveform tracing can provide information beyond timely BP measurements. For example, the slope of the arterial upstroke correlates with the derivative of pressure over time, dP/dt, and thus gives an indirect estimate of myocardial contractility. This is not specific information, because an increase in SVR alone will also result in an increase in the slope of the upstroke. The arterial waveform can also present a visual estimate of the hemodynamic consequences of arrhythmias, and the arterial pulse contour can be used to estimate stroke volume and cardiac output. Additionally, hypovolemia is suggested

when the arterial pressure shows large SBP variation during the respiratory cycle in the mechanically ventilated patient (also see previous discussion).80,81

Contraindications Some of the contraindications for noninvasive BP monitoring include prior ipsilateral mastectomy with lymphadenectomy, burns, and cutaneous infections. Contraindications to arterial cannulation include local infection, proximal obstruction, vasoocclusive disorders, and surgical considerations. Coagulopathic patients frequently require invasive BP monitoring, and more central arterial cannulation may result in significant hematoma formation. Thus, in anticoagulated and coagulopathic patients, it is recommended that more peripheral arterial cannulation sites be used when this form of monitoring is required. Anatomic factors may lead to intraarterial pressure readings that markedly underestimate the central aortic pressure. The thoracic outlet syndrome and congenital anomalies of the aortic arch vessels will obstruct flow to the upper extremities. Aortic coarctation will diminish flow to the lower extremities. Arterial pressure distal to a previous arterial cutdown site may be lower than the central aortic pressure owing to arterial stenosis at the cutdown site. Patients with a prior classic Blalock-Taussig shunt typically have lower BP readings on the upper extremity distal to the shunt. The opposite site should be chosen for arterial BP monitoring. Radial and brachial arterial cannulation is contraindicated in patients with a history of Raynaud syndrome or Buerger disease (thromboangiitis obliterans). This is especially important in the perioperative setting, because hypothermia of the hand is the main trigger for vasospastic attacks in Raynaud syndrome.82 It is recommended that large arteries, such as the femoral or axillary arteries, be used for intraarterial monitoring if indicated in patients with either of these diseases. Several surgical maneuvers may interfere with intraarterial monitoring. During mediastinoscopy, the scope intermittently compresses the innominate artery against the manubrium. In this situation, it is advantageous to monitor radial artery pressure on one side, while a pulse oximeter probe may be placed on the opposite extremity. Invasive BP monitoring on the right extremity allows immediate recognition of innominate artery compression. Alternatively, the pulse oximeter waveform displayed by most modern pulse oximeter devices allows the recognition of innominate artery compression. The invasive BP can then continuously be measured on the opposite side.

References 1. O’Brien E, Waeber B, Parati G, et al. Blood pressure measuring devices: recommendations of the European Society of Hypertension. BMJ 2001;322:531–6.

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2. Young C, Mark J, White W, et al. Clinical evaluation of continuous noninvasive blood pressure monitoring: Accuracy and tracking capabilities. J Clin Monit 1995;11:245–52. 3. Pittman JA, Ping JS, Mark JB. Arterial and central venous pressure monitoring. Int Anesthesiol Clin 2004;42:13–30. 4. Kleinman B. Understanding natural frequency and damping and how they relate to the measurement of blood pressure. J Clin Monit 1989;5:137–47. 5. Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood pressure measurements in humans and experimental animals. Part 1: Blood pressure measurement in humans: a statement for professionals from the Subcommittee of Professional and Public Education of the American Heart Association Council on High Blood Pressure Research. Circulation 2005;111:697–716. 6. Pickering TG, Hall JE, Appel LJ, et al. Recommendations for blood pressure measurements in humans: an AHA Scientific Statement from the Council on High Blood Pressure Research Professional and Public Education Subcommittee. J Clin Hypertension 2005;7:102–107. 7. O’Brien E, Petrie J, Littler WA, et al. The British Hypertension Society Protocol for the evaluation of blood pressure measuring devices. J Hypertens 1993;11:S43–63. 8. American National Standard. Electronic or automated sphygmomanometers. ANSI/AAMI SP10–1992. Arlington, VA: Association for the Advancement of Medical Instrumentation, 1993, p. 40. 9. Friedman BA, Alpert BS, Osborn D, et al. Assessment of the validation of blood pressure monitors: a statistical reappraisal. Blood Press Monit 2008;13:187–91. 10. Parati G, Ongaro G, Bilo G, Glavina F. Non-invasive beat-to-beat blood pressure monitoring: new developments. Blood Press Monit 2003;8:31–6. 11. Belani K, Ozaki M, Hynson J, et al. A new noninvasive method to measure blood pressure: results of a multicenter trial. Anesthesiology 1999;91:686–92. 12. Pe˜na´z J. Photoelectric measurement of blood pressure volume and flow in the finger. In Digest of the 10th International Conference on Medical and Biological Engineering, Dresden, 1973, p. 104. 13. Wesseling KH, De Wit B, Van Der Hoeven GMA, van Goudoever J, Settels JJ. Physiocal, calibrating finger physiology for Finapres. Homeostasis 1995;36:67–82. 14. Wesseling KH, Jansen JR, Settels JJ, Schreuder JJ. Computation of aortic flow from pressure in humans using a nonlinear, three-element model. J Appl Physiol 1993;74:2566–73. 15. Kurki TS, Sanford TJ, Smith NT, Dec-Silver H, Head N. Effects of radial artery cannulation on the function of finger blood pressure and pulse oximeter monitors. Anesthesiology 1988;69:778–82. 16. Kurki TS, Piirainen HI, Kurki PT. Non-invasive monitoring of finger arterial pressure in patients with Raynaud’s phenomenon: effects of exposure to cold. Br J Anaesth 1990;65:558–63. 17. Kurki T. Continuous noninvasive monitoring of arterial blood pressure in the emergency department. Am J Noninv Cardiology 1991;5:103–5. 18. Bos WJW, Van Den Meiracker AH, Wesseling KH, Schalekamp MAH. Effect of regional and systemic changes in vasomotor tone on finger pressure amplification. Hypertension 1995;26: 315–20. 19. Bos WJW, van Goeoever J, van Montfrans GA, Van Den Meiracker AH, Wesseling KH. Reconstruction of brachial artery

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in patients with reduced cardiac function. Crit Care Med 2003;31:1399–404. Michard F. Changes in arterial pressure during mechanical ventilation. Anesthesiology 2005;103:419–28. Kleinman B. Understanding natural frequency and damping and how they relate to the measurement of blood pressure. J Clin Monit 1989;5:137–47. Barbeito A, Mark JB. Arterial and central venous pressure monitoring. Anesthesiol Clin 2006;24:717–35. Boutros A, Albert S. Effect of the dynamic response of transducer–tubing system on accuracy of direct blood pressure measurement in patients. Crit Care Med 1983;11: 124–7. Todorovic M, Jensen EW, Thogersen C. Evaluation of dynamic performance in liquid-filled catheter systems for measuring invasive blood pressure. Int J Clin Monit Comput 1996; 13:173–8. Heimann PA, Murray WB. Construction and use of catheter-manometer systems. J Clin Monit 1993;9:45–53. Kleinman B, Frey K, Stevens R. The fast flush test – is the clinical comparison equivalent to its in vitro simulation? J Clin Monit Comput 1998;14:485–9. Kleinman B, Powell S, Kumar P, et al. The fast flush test measures the dynamic response of the entire blood pressure monitoring system. Anesth 1992;77:1215–20. Schwid HA. Frequency response evaluation of radial artery catheter–manometer systems: sinusoidal frequency analysis versus flush method. J Clin Monit 1988;4:181–5. Gibbs NC, Gardner RM. Dynamics of invasive pressure monitoring systems: clinical and laboratory evaluation. Heart Lung 1988;17:43–51. Staessen JA, Asmar R, De Buyzere M, et al. Task Force II: Blood pressure measurement and cardiovascular outcome. Blood Press Monit 2001;6:355–70. Aronson S, Fontes ML. Hypertension: a new look at an old problem. Curr Opin Anaesthesiol 2006;19:59–64. Fontes ML, Aronson S, Mathew JP, et al. Pulse pressure and risk of adverse outcome in coronary bypass surgery. Anesth Analg 2008;107:1103–6. Aronson S, Boisvert D, Lapp W. Isolated systolic hypertension is associated with adverse outcomes from coronary artery bypass grafting surgery. Anesth Analg. 2002;94:1079–84. Kheterpal S, O’Reilly M, Englesbe MJ, et al. Preoperative and intraoperative predictors of cardiac adverse events after general, vascular, and urological surgery. Anesthesiology 2009;110: 58–66. Singleton K, Brady G, Lai S, et al. The Australian Incident Monitoring Study. Problems associated with vascular access: an analysis of 2000 incident reports. Anaesth Intensive Care 1993;21:664–669. Khalifa R, Dahyot-Fizelier C, Laksiri L, et al. Indwelling time and risk of colonization of peripheral arterial catheters in critically ill patients. Intensive Care Med 2008;34:1820–6. Band JD, Maki DG. Infection caused by arterial catheters used for hemodynamic monitoring. Am J Med 1979;67:735–41. Shinozaki T, Deane R, Mazuzan JE, et al. Bacterial contamination of arterial lines: A prospective study. JAMA 1983;249:223–5. Weinstein RA, Stamm WE, Kramer L. Pressure monitoring devices: overlooked sources of nosocomial infection. JAMA 1976;236:936–8.

60. Stamm WE, Colella JJ, Anderson RL, et al. Indwelling arterial catheters as a source of nosocomial bacteremia. N Engl J Med 1975;292:1099–1102. 61. Koh DB, Gowardman JR, Rickard CW, et al. Prospective study of peripheral arterial catheter infection and comparison with concurrently sited central venous catheters. Crit Care Med 2008;36:397–402. 62. Traore O, Liotier J, Souweine B. Prospective study of arterial and central venous catheter colonization and of arterial- and central venous catheter-related bacteremia in intensive care units. Crit Care Med 2005;33:1276–80. 63. Rijnders BJ, Van Wijngaerden E, Wilmer A, Peetermans WE. Use of full sterile barrier precautions during insertion of arterial catheters: a randomized trial. Clin Infect Dis 2003;36: 743–8. 64. Sherertz RJ. Update on vascular catheter infections. Curr Opin Infect Dis 2004;17:303–7. 65. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections. The Hospital Infection Control Practices Advisory Committee, Center for Disease Control and Prevention. Pediatrics 2002;110:e51. 66. Scheer B, Perel A, Pfeiffer UJ. Clinical review: complications and risk factors of peripheral arterial catheters used for haemodynamic monitoring in anaesthesia and intensive care medicine. Crit Care 2002;6:199–204. 67. Bedford RF, Wollman H. Complications of percutaneous radial artery cannulation: An objective prospective study in man. Anesthesiology 1973;38:228–36. 68. Bedford RF. Radial arterial function following percutaneous cannulation with 18- and 20-gauge catheters. Anesthesiology 1977;47:37–39. 69. Bedford RF. Wrist circumference predicts the risk of radial arterial occlusion after cannulation. Anesthesiology 1978;48:377–8. 70. Wong AY, O’Regan AM. Gangrene of digits associated with radial artery cannulation. Anaesthesia 2003;58:1034–5. 71. Green JA, Tonkin MA. Ischaemia of the hand in infants following radial or ulnar artery catheterisation. Hand Surg 1999;4:151–7. 72. Bright E, Baines DB, French BG, et al. Upper limb amputation following radial artery cannulation. Anaesth Intensive Care 1993;21:351–3. 73. Kim JM, Arakawa K, Bliss J. Arterial cannulation: Factors in the development of occlusion. Anesth Analg 1975;54:836–41. 74. Chang C, Dughi J, Shitabata P, et al. Air embolism and the radial arterial line. Crit Care Med 1988;16:141–3. 75. Lowenstein E, Little JW, Lo HH. Prevention of cerebral embolization from flushing radial artery cannulae. N Engl J Med 1971;285:1414–5. 76. Zavela NG, Gravlee GP, Bewckart DH, et al. Unusual cause of hypotension after cardiopulmonary bypass. J Cardiothorac Vasc Anesth 1996;10:553–6. 77. Qvist J, Peterfreund R, Perlmutter G. Transient compartment syndrome of the forearm after attempted radial artery cannulation. Anesth Analg 1996;83:183–5. 78. Edwards DP, Clarke MD, Barker P. Acute presentation of bilateral radial artery pseudoaneurysms following arterial cannulation. Eur J Vasc Endovasc Surg 1999;17:456–7. 79. Knight CG, Healy DA, Thomas RL. Femoral artery pseudoaneurysms: risk factors, prevalence, and treatment options. Ann Vasc Surg 2003;17:503–8.

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80. Rooke GA, Schwid HA, Shapira Y. The effect of graded hemorrhage and intravascular volume replacement on systolic pressure variation in humans during mechanical and spontaneous ventilation. Anesth Analg 1995;80: 925–32.

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81. Gunn SR, Pinsky MR. Implications of arterial pressure variation in patients in the intensive care unit. Curr Opin Crit Care 2001;7:212–7. 82. Porter JM. Raynaud’s syndrome. In Sabiston DC, ed. Textbook of Surgery. Philadelphia: W. B. Saunders, 1985, pp. 1925–32.

Chapter

7

Central venous and pulmonary artery catheterization Deborah Dubensky and Alexander J. C. Mittnacht

Introduction Currently, percutaneous central venous cannulation is performed in more than five million patients in the United States annually.1 Pulmonary artery catheter (PAC) use, after its clinical introduction in the early 1970s, has decreased significantly in the past decade and has been reported in 2 percent of all medical admissions in the United States.2 The incidence of right heart (PAC) catheterization varies significantly between institutions and hospital settings; even national and international differences have been reported without any apparent difference in patient outcome. This chapter provides an overview of central venous cannulation and right heart catheterization with a critical review of current standards and recommendations.

Technical concept Techniques and insertion sites Central venous cannulation may be accomplished by catheterthrough-needle, catheter-over-needle, or catheter-over-wire (Seldinger) techniques, the last being used most frequently outside the catheterization laboratory. The considerations for selecting the site of cannulation include the experience of the operator, ease of access, anatomic anomalies, and the ability of the patient to tolerate the position required for catheter insertion. The most frequently used sites of insertion are the internal jugular vein, subclavian vein, femoral vein, external jugular vein, and large antecubital peripheral veins. Even though the internal jugular approach to central venous cannulation is the most popular, for reasons to be described, other sites may be preferable, considering individual patient characteristics or the particular indication for central venous cannulation. Cannulation of the internal jugular vein (IJV) was first described by English and colleagues in 1969.3 Advantages of this technique include (1) the high success rate as a result of the relatively predictable relationship of the anatomic structures; (2) a short, straight course to the right atrium (RA) that almost always ensures positioning of the catheter tip in the RA or superior vena cava (SVC); (3) easy access from the head of the oper-

ating room table; and (4) fewer complications than with subclavian vein catheterization. The IJV is located under the medial border of the lateral head of the sternocleidomastoid (SCM) muscle. The carotid artery is typically located deeper and more medial to the IJV; however, the use of ultrasound-guided central cannulation has revealed a much less consistent relationship between the two vessels. The right IJV is preferred, because this vein takes the straightest course into the SVC, the right cupola of the lung may be lower than the left, and the thoracic duct is located on the left side.4 There are several approaches to right IJV cannulation described in the literature. The close relationship of the IJV to structures such as the carotid artery mandates a technique that poses the lowest risk to the patient. The use of a small-caliber “finder” needle may prevent puncture of the carotid artery with large-bore needles. The use of ultrasound-guided cannulation of large central veins has been advocated and has shown to increase success rate and decrease the incidence of certain complications (as discussed later). The needle should be placed at the apex of the triangle formed by the two heads of the SCM muscle at a 45-degree angle to the skin, and directed toward the ipsilateral nipple. If venous blood return is not obtained, the needle is withdrawn to the subcutaneous tissue and then passed in a more lateral or medial direction until the vein is located. After the catheter is advanced into the vein, the needle is removed, and the proper intravenous position must be determined. To confirm that an artery has not been inadvertently cannulated, comparison of the color of the blood sample to an arterial sample drawn simultaneously has been described.5 However, manometry is the preferred method of confirmation. Intravenous tubing attached to the catheter passively fills with blood when lowered below the heart and subsequently recedes to typical central venous pressure (CVP) levels with respiratory variation when held above the heart. Transduction of the pressure waveform is another technique that has been recommended.6,7 In specific settings such as the cardiac operating room, the placement of a transesophageal echocardiography probe prior to IJV cannulation can help confirm intravenous positioning of the guidewire in the right atrium before a largebore cannula is advanced.

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Monitoring in Anesthesia and Perioperative Care

Ultrasonic guidance of IJV cannulation Ultrasound has been increasingly used to define the anatomic variations of the IJV.8 Even though most commonly used for IJV cannulation, it can be useful in cannulating veins at other sites, as well as for arterial cannulation. Recently, a review and meta-analysis of randomized controlled trials looking at ultrasound-guided central venous cannulation found that realtime two-dimensional ultrasound for IJV cannulation in adults had a significantly higher success rate overall and on the first attempt, compared with the landmark method.9 In 2005, Leyvi and associates10 showed a higher success rate in IJV cannulation in children with the use of ultrasound compared with the traditional landmark technique, without any difference in complications. Even though most publications including prospective studies advocate the use of ultrasound for IJV cannulation in infants and children,11–14 a few studies have shown no difference or even an increased risk of complications with ultrasound use compared with the landmark technique.15,16 Overall, most studies have demonstrated that two-dimensional ultrasonic guidance of IJV cannulation is helpful in locating the vein, permits more rapid cannulation, and decreases the incidence of arterial puncture.17–24 Circumstances under which ultrasonic guidance of IJV cannulation can be advantageous include patients with difficult neck anatomy (e.g. short neck, obesity), hypovolemia, prior neck surgery or radiation treatment; anticoagulated patients; and infants.25 Additionally, ultrasound has provided more precise data regarding the structural relationship between the IJV and the carotid artery. Troianos and coworkers found that in more than 54 percent of patients, more than 75 percent of the IJV overlies the carotid artery.26 Patients who were over the age of 60 were more likely to have this type of anatomy. In pediatric patients, Alderson and associates found that the carotid artery coursed directly posterior to the IJV in 10 percent of patients.27 Sulek and colleagues observed that there was greater overlap of the IJV and the carotid artery when the head is rotated 80 degrees toward the contralateral side compared with head rotation of only 0 to 40 degrees.28 The percentage overlap was larger on the left side of the neck compared with the right. Therefore, excessive rotation of the head of the patient toward the contralateral side may distort the normal anatomy in a manner that increases the risk of inadvertent carotid artery puncture. Doppler/ultrasound has also been used to demonstrate that the Valsalva maneuver increases IJV cross-sectional area by approximately 25 percent,29 and that the Trendelenburg position increases it by approximately 37 percent.30 Suarez and colleagues concluded that the lateral access approach to the internal jugular vein yielded the largest target area.31 Parry recently published a study showing that maximal right IJV diameter can be achieved by placing the patient in 15 degrees Trendelenburg position, slightly elevating the head with a small pillow, keeping the head close to midline, and releasing the pressure administered to palpate the carotid artery prior to IJV cannulation.32

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Figure 7.1. Typical relationship between right IJV and carotid artery in the transverse imaging approach. Note that part of the IJV is located above the carotid artery. Slight pressure with the transducer head compresses the IJV compared with the carotid artery. It is important to always demonstrate both IJV and carotid artery to clearly identify the IJV.

At the time of this writing, ultrasonic guidance is not yet the standard of care for IJV cannulation. However, many institutions have departmental policies in place that require ultrasound-guided IJV cannulation, particularly in anticoagulated patients and/or patients with difficult anatomy. The accumulating evidence cited here should be sufficient to justify the cost and effort related to acquiring the equipment and training anesthesiologists in its use. As with most emerging techniques, the practitioner must gain experience in a number of normal IJV cannulations to gain most benefit from the technology in the more complicated patient. Figure 7.1 shows the typical image obtained during two-dimensional ultrasound-guided IJV cannulation.

External jugular vein Although the external jugular vein (EJV) is another means of reaching the central circulation, the success rate with this approach is lower because of the tortuous path followed by the vein. In addition, a valve is usually present at the point at which the EJV perforates the fascia to join the subclavian vein (SCV). One study, however, reported a success rate of 90 percent using a J-wire to manipulate past obstructions into the central circulation.33 The main advantage of this technique is that there is no need to advance a needle into the deeper structures of the neck. Manipulation of the shoulder and rotation of the guidewire between the operator’s fingers may be useful maneuvers when difficulty is encountered in passing the wire into the SVC.

Subclavian vein The subclavian vein is readily accessible from supraclavicular or infraclavicular approaches and has long been used for central venous access.34 The success rate is higher than the EJV approach, but lower than the right IJV approach. Cannulation of the subclavian vein is associated with a higher incidence

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

junction and are used for the aspiration of air emboli in neurosurgical patients. Because of problems inherent with intravascular electrocardiography, Mongan and colleagues described a method for transducing the pressure waveform and identifying the point at which the catheter tip entered the right ventricle.45 They then calculated the distance required to withdraw the catheters to the SVC–RA junction (for three different types of air-embolism–aspirating catheters). Others have used transesophageal echocardiography (TEE) to assist in the correct placement of these types of catheters.46 Even though peripherally placed central venous catheters avoid the placement of needles into deep venous structures, there are still significant risks associated with their use.47–50

of complications, especially the risk of a pneumothorax, compared with the IJV approach. Other complications associated with SCV cannulation are arterial punctures, misplacement of the catheter tip, aortic injury, cardiac tamponade, mediastinal hematoma, and hemothorax.35–38 The SCV may be the cannulation site of choice, however, when CVP monitoring is indicated in patients who have contraindications to IJV cannulation. It is also useful for parenteral nutrition or for prolonged central venous access because the site is easier to maintain and is well tolerated by patients. The infraclavicular approach is performed with the patient supine or in the Trendelenburg position with a folded sheet between the scapulae to increase the distance between the clavicle and the first rib. The head is turned to the contralateral side. A thin-walled needle or intravenous catheter is inserted 1 cm below the midpoint of the clavicle, the needle is “walked” along the anterior border of the clavicle, and, once the inferior aspect of the clavicle has been reached, the needle is directed toward the suprasternal notch under the posterior surface of the clavicle. When free-flowing venous blood is obtained, the guidewire is passed into the SCV and is exchanged for a CVP catheter. Kinking of the catheter because of the course underneath the clavicle occurs more frequently compared with RIJ cannulation. The supraclavicular approach is performed with the patient in the Trendelenburg position with the head turned away from the side of the insertion. The finder needle is inserted at the lateral border of the SCM at the point of insertion into the clavicle. The needle is directed to bisect the angle between the SCM and the clavicle, about 15 to 20 degrees posteriorly. The vessel is very superficial (about 1 to 2 cm) and lies very close to the innominate artery and the pleura. There is an increased risk of an injury to the thoracic duct during the left-sided approach.

The femoral vein is less frequently cannulated in the adult patient for intraoperative monitoring purposes. However, cannulation of this vein is technically simple, and the success rate is high. Cannulation of the vessel should be done about 1 to 2 cm below the inguinal ligament. The vein typically lies medial to the artery. Although older literature reported a high rate of catheter sepsis and thrombophlebitis with this approach, this may no longer be valid with increasing awareness of using a full sterile technique, disposable catheter kits, and improved catheter technology.51,52 Subcutaneous tunneling of femoral central venous catheters has been suggested to reduce the incidence of catheterrelated infections.53,54 In patients with SVC obstruction, or other contraindications to IJV or SCV cannulation, the femoral vein is necessary for intravenous access and to obtain a true CVP measurement. The catheter should be long enough so that the tip lies within the mediastinal portion of the inferior vena cava.

Antecubital veins

Pulmonary artery catheterization

Another route for central venous monitoring is via the basilic or cephalic veins. The advantages of this approach are the low likelihood of complications and the ease of access intraoperatively if the arm is exposed. The major disadvantage is that it is often difficult to ensure placement of the catheter in a central vein. Studies have indicated that blind advancement will result in central venous cannulation in 59 percent to 75 percent of attempts.39,40 Chest radiographs are usually necessary to confirm that the tip of the catheter has been placed appropriately; this involves some time delay. Alternatively, the guidewire can be attached to a specially designed ECG adapter; a change of the ECG waveform confirms proper positioning. Exact positioning of the catheter tip is crucial, as movement of the arm will result in significant catheter migration and could cause cardiac tamponade.41–43 Unsuccessful attempts result most frequently from failure to pass the catheter past the shoulder, or retrograde cannulation of the ipsilateral IJV. Turning the head toward the ipsilateral side may help prevent IJV placement of the catheter.44 These catheters are positioned at the SVC–RA

The considerations for the insertion site of a PAC are the same as for CVP catheters. The right IJV approach remains the technique of choice because of the direct path between this vessel and the RA. In patients undergoing cardiac surgery, the placement of a large-bore introducer sheath and PAC via the SCV may be complicated by kinking of the catheter when the sternum is retracted.55 Passage of the PAC from the percutaneous insertion site to the PA can be accomplished by monitoring the pressure waveform from the distal port of the catheter, or under fluoroscopic guidance. Waveform monitoring is the more common technique for perioperative right heart catheterization. First, the catheter must be advanced through the vessel introducer (15– 20 cm) before inflating the balloon. The inflation of the balloon facilitates further advancement of the catheter through the RA and right ventricle (RV) into the pulmonary artery. Normal intracardiac pressures are shown in Table 7.1. The pressure waveforms seen during advancement of the PAC are illustrated in Figure 7.2.

Femoral vein

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Monitoring in Anesthesia and Perioperative Care

Table 7.1.

Normal intracardiac pressures (mmHg)

Location

Mean

Range

Right atrium Right ventricle Pulmonary arterial systolic/diastolic Mean pulmonary arterial Pulmonary capillary wedge pressure Left atrial pressure Left ventricular end-diastolic pressure Left ventricular systolic pressure

5 25/5 23/9 15 10 8 8 130

1–10 15–30/0–8 15–30/5–15 10–20 5–15 4–12 4–12 90–140

The RA waveform is seen until the catheter tip crosses the tricuspid valve and enters the RV. In patients with prior tricuspid valve ring annuloplasty, significant tricuspid regurgitation, or tricuspid stenosis, advancing the catheter past the tricuspid valve (TV) can become cumbersome and, in rare cases, even impossible. Trendelenburg positioning places the RV superior to the RA and, thus, may aid in advancing the PAC past the TV. TEE guidance can prove invaluable in these cases. The experienced echocardiographer can position the catheter tip just proximal to the TV orifice. Further attempts to get past the TV require much less catheter manipulation. Once the catheter is advanced into the RV, there is a sudden increase in systolic pressure, but little change in diastolic pressure compared with the RA tracing. Arrhythmias, particularly premature ventricular complexes, usually occur at this point, but almost always resolve without treatment once the catheter tip has crossed the pulmonary valve. The catheter is rapidly advanced through the RV toward the PA. Slight reverse Trendelenburg and right lateral decubitus position brings the right ventricular outflow tract anteriorly and superior to the RV and, thus, aids in advancing the catheter into the PA.56 As the catheter crosses the pulmonary valve, a dicrotic notch appears in the pressure waveform, and there is a sudden increase in diastolic pressure. The pulmonary capillary wedge pressure (PCWP) – or, more accurately, pulmonary artery occlusion pressure (PAOP) – tracing is obtained by advancing the catheter approximately 3 to 5 cm farther until there is a change in the waveform associated with a drop in the measured

RA

RV

PA

PCW

Figure 7.2. The waveforms encountered during the flotation of a pulmonary artery catheter from the venous circulation to the pulmonary capillary wedge (PCW) position. Note the sudden increase in systolic pressure as the catheter enters the right ventricle (RV), the sudden increase in diastolic pressure as the catheter enters the pulmonary artery (PA), and the decrease in mean pressure as the catheter reaches the PCW position. RA = right atrium. With permission from Reich DL, Mittnacht A, London M, Kaplan JA. Monitoring of the heart and vascular system. In Kaplan JA, Reich DL, Lake CL, Konstadt SL, eds. Kaplan’s Cardiac Anesthesia, 5th ed. Philadelphia: Saunders Elsevier; 2006, pp. 385–436 (figure 14-13).

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mean pressure. Deflation of the balloon results in reappearance of the PA waveform and an increase in the mean pressure value. Benumof and coworkers found that most catheters pass into the right middle or lower lobes.57 Using the right IJV approach, the RA is entered at 25 to 35 cm, the RV at 35 to 45 cm, the PA at 45 to 55 cm, and the PCWP at 50 to 60 cm in the vast majority of patients. If the catheter does not enter the PA by 60 cm, the balloon should be deflated and it should be withdrawn into the RA, and another attempt should be made to advance the catheter into proper position. Excessive coiling of the catheter in the RV should be avoided to prevent catheter knotting. The balloon should be inflated for only short periods of time to measure the PCWP. The PA waveform should be monitored continually to be certain that the catheter does not float out into a constant wedge position, because this may lead to pulmonary artery rupture and/or pulmonary infarction. The PAC is covered by a sterile sheath that must be secured at both ends to prevent contamination of the external portion of the catheter. Not infrequently, the PAC must be withdrawn a short distance as extra catheter in the RV floats out more peripherally into the PA over a period of time as the catheter softens, and during cardiac surgery when manipulation of the heart and cardiopulmonary bypass typically lead to spontaneous wedging of the catheter tip. The time for the entire PAC insertion procedure is less than 10 minutes in experienced hands. Whether the PAC should be placed prior to anesthesia induction or after the patient has been anesthetized is a matter of personal and institutional preference. However, because the vast majority of outcome studies failed to show any benefit from PAC placement, insertion of a PAC in an awake patient should be considered carefully. Unless the position of the PAC can be confirmed with TEE, a chest radiograph should be obtained postoperatively in all patients to check the position of the PAC.

Parameters monitored Central venous pressure CVP catheters are used to measure the filling pressure of the RV, give an estimate of the intravascular volume status, and assess right ventricular function. For accurate pressure measurement, the distal end of the catheter must lie within one of the large intrathoracic veins or the RA. In any pressure monitoring system, it is necessary to have a reproducible landmark (such as the midaxillary line) as a zero reference. This is especially important in monitoring venous pressures, because small changes in the height of the zero reference point produce proportionately larger errors on the venous pressure scale compared with ... in arterial pressure monitoring. The normal CVP waveform consists of three upward deflections (A, C, and V waves) and two downward deflections (X and Y descents) (see Figure 7.3). The A wave is produced by right atrial contraction and occurs just after the P wave on the ECG. The C wave occurs as a

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

Figure 7.3. The relationship of the central venous pressure (CVP) tracing to the electrocardiogram (ECG) in normal sinus rhythm. The normal CVP waveform consists of three upward deflections (A, C, and V waves) and two downward deflections (X and Y descents). Adapted with permission from reference. 78, figure 2.

R T

P ECG

DIASTOLE

SYSTOLE A C

A

α

CVP X

Y

result of isovolumic ventricular contraction forcing the tricuspid valve to bulge upward into the right atrium. The pressure within the RA then decreases as the tricuspid valve is pulled away from the atrium during right ventricular ejection, forming the X descent. The RA continues to fill during late ventricular systole, forming the V wave. The Y descent occurs when the tricuspid valve opens and blood from the RA empties rapidly into the RV during early diastole. It is important to remember that many peaks and troughs in the CVP waveform are created artifactually from the transducer–tubing monitoring system. In tachycardic patients, the A and C waves can blend and may not be easily distinguishable. The CVP waveform may be useful in the diagnosis of pathologic cardiac conditions. For example, onset of an irregular rhythm and loss of the A wave suggest atrial flutter or fibrillation. Cannon A waves occur as the RA contracts against a closed tricuspid valve as in junctional (atrioventricular [AV] nodal) rhythm, complete heart block, and ventricular arrhythmias (see Figure 7.4). This is clinically relevant because nodal rhythms are frequently seen during anesthesia and may produce hypotension owing to a decrease in stroke volume. Cannon A waves may also be present when there is increased resistance to RA emptying, as in tricuspid stenosis, right ventricular hypertrophy, pulmonary stenosis, or pulmonary hypertension. Early systolic or holosystolic cannon V waves (or CV waves) occur if there is a significant degree of tricuspid regurgitation (see Figure 7.4). Large V waves may also appear later in systole if the ventricle becomes noncompliant as a result of ischemia or right ventricular failure.58 Pericardial constriction produces characteristic waveforms in the CVP tracing (see Figure 7.5). There is a decrease in venous return owing to the inability of the heart chambers to dilate because of the constriction. This causes prominent A and V waves and steep X and Y descents (creating an “M” configuration) resembling that seen with diseases that cause decreased right ventricular compliance. Egress of blood from the RA to

the RV is initially rapid during early diastolic filling of the RV (creating a steep Y descent), but is short-lived and abruptly halted by the restrictive, noncompliant RV. The RA pressure then increases rapidly and reaches a plateau until the end of the A wave, at the end of diastole. With pericardial tamponade, the X descent is steep but the Y descent is not present, because early diastolic runoff is impaired by the pericardial fluid collection.

PAC The PCWP waveform is analogous to the CVP waveform described previously. The A, C, and V waves are similarly timed in the cardiac cycle. Large V waves have been described during mitral regurgitation, LV diastolic noncompliance, and episodes of myocardial ischemia.59 They are seen on the PCWP tracing as large (or “giant”) V waves that occur slightly later than the upstroke on the PA tracing.60 They can also be identified on the PA waveform tracing, causing the PA waveform to become wider, and the dicrotic notch may be lost. The occurrence of V waves in patients with severe mitral regurgitation has been studied in detail by Grose and colleagues.61 They found that in some patients severe mitral regurgitation causes reversal of semilunar valve closure. Early pulmonic valve closure with the dicrotic notch in the pulmonary artery V wave preceding the aortic dictrotic notch could be demonstrated in patients with low pulmonary vascular resistance (also see Figures 7.6 and 7.7). The etiology of large V waves during myocardial ischemia is probably caused by a decrease in diastolic ventricular compliance. Alternatively, they may be caused by mitral regurgitation induced by ischemic papillary muscle dysfunction. In this instance, the V waves may occur earlier during the onset of the C wave (CV wave). Large V waves, however, have not been shown to correlate well with other determinants of myocardial ischemia.62,63 Specific information that can be gathered from the PAC and the quantitative measurements of cardiovascular and pulmonary function that can be derived from this information are listed in Tables 7.2 and 7.3.

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Figure 7.5. Pericardial constriction produces a central venous pressure trace (bottom) that displays tall A and V waves and steep systolic X and diastolic Y descents. The electrocardiogram (top) and arterial blood pressure (middle) traces are also shown. Adapted with permission from Pittman JAL, Ping JS, Mark JB. Arterial and central venous pressure monitoring. Int Anesthesiol Clin 2004;42:13–30, figure 10.

IABP ON

Cannon A wave

Regurgitant CV wave

Figure 7.4. Central venous pressure (CVP) waveform in a patient with junctional rhythm (cannon A waves) and in a patient with tricuspid regurgitation (CV wave). The electrocardiogram (top), arterial blood pressure (middle), and CVP (bottom) traces are shown. Adapted with permission from Pittman JAL, Ping JS, Mark JB. Arterial and central venous pressure monitoring. Int Anesthesiol Clin 2004;42:13–30, figure 9.

100 mmHg

75

One of the main reasons that clinicians measure PCWP and pulmonary artery diastolic pressure (PAD) is that these parameters are estimates of left atrial pressure (LAP), which, in turn, is an estimate of left ventricular end-diastolic pressure (LVEDP). Left ventricular end-diastolic pressure is an index of left ventricular end-diastolic volume (LVEDV), which correlates well with left ventricular preload.64 The relationship between LVEDP and LVEDV is described by the left ventricular compliance curve. This nonlinear curve is affected by many factors, such as ventricular hypertrophy and myocardial ischemia.65,66 Thus, the PCWP and PAD do not directly measure left ventricular preload. The relationship of these parameters is diagrammed in Figure 7.8.

62

DN PA DN

50

y wave PA

y wave RV

25 PCW

B

Figure 7.6. V waves can be seen on the PCWP tracing (left) and pulmonary artery pressure tracing in patients with severe mitral regurgitation. PA = pulmonary artery, PCW = pulmonary capillary wedge, RV = right ventricular, DN = dicrotic notch. With permission from reference 61, figure 1B.

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

Table 7.3.

Oxygenation parameters

Formula

mmHg

DN

100

AO

75

50

DN

V wave PA RV

25 0

Figure 7.7. Micromanometer pressure tracings from a patient with severe mitral regurgitation. In the main pulmonary artery, a V wave of 50 mmHg is present, which exceeds peak right ventricular or pulmonary artery systolic pressure by 7 mmHg. The incisura of the pulmonary artery dictrotic notch precedes aortic dictrotic notch by 15 msec. With permission from Reference 61, Figure 2.

Table 7.2.

Hemodynamic parameters

Formula

Normal Values

Cardiac index CI = CO/BSA Stroke volume SV = CO ∗1000/HR Stroke index SI = SV/BSA Left ventricular stroke work index LVSWI = 1.36 ∗ (MAP – PCWP) ∗ SI/100 Right ventricular stroke work index RVSWI = 1.36 ∗ (MPAP – CVP) ∗ SI/100 Systemic vascular resistance SVR = (MAP – CVP) ∗ 80/CO Systemic vascular resistance index SVRI = (MAP – CVP) ∗ 80/CI Pulmonary vascular resistance PVR = (MPAP – PCWP) ∗ 80/CO Pulmonary vascular resistance index PVRI = (MPAP – PCWP) ∗ 80/CI

2.8–4.2 l/min/m2 50–110 mL (per beat) 30–65 mL/m2 45–60 gram-meters/m2 5–10 gram-meters/m2

Normal Values

Arterial O2 content CaO2 = (1.39 ∗ Hb ∗ SaO2) + (0.0031 ∗ PaO2) Mixed venous O2 content CvO2 = 1.39 ∗ Hb ∗ SvO2 + 0.0031 ∗ PvO2 Arteriovenous O2 content difference avDO2 = CaO2 – CvO2 Pulmonary capillary O2 content CcO2 = 1.39 ∗ Hb ∗ ScO2 + 0.0031 ∗ PcO2 Pulmonary shunt fraction Qs/Qt = 100 ∗ (CcO2 – CaO2)/(CcO2 – CvO2) O2 delivery DO2 = 10 ∗ CO ∗ CaO2 O2 consumption VO2 = 10 ∗ CO ∗ (CaO2 – CvO2)

18–20 mL/dL 13–16 mL/dL 4–5.5 mL/dL 19–21 mL/dL 2–8 percent 800–1100 mL/min 150–300 mL/min

Hb = Hemoglobin; SvO2 = venous oxygen saturation; PvO2 venous oxygen tension; ScO2 = pulmonary capillary oxygen saturation; PcO2 = pulmonary capillary oxygen tension. From McGrath R. Invasive bedside hemodynamic monitoring. Prog Cardiovasc Dis 1986;29:129. With permission from Reich DL, Mittnacht A, London M, Kaplan JA. Monitoring of the heart and vascular system. In Kaplan JA, Reich DL, Lake CL, Konstadt SL (eds.) Kaplan’s Cardiac Anesthesia 5th ed. Philadelphia: Saunders Elsevier, 2006, pp. 385–436 (table 14-3).

The PCWP and PAD pressures will not accurately reflect LVEDP in the presence of incorrect positioning of the PAC catheter tip, pulmonary vascular disease, high levels of positive end expiratory pressure (PEEP), or mitral valvular disease. The patency of vascular channels between the distal port of the PAC and the left atrium (LA) is necessary to ensure a close relationship between the PCWP and LAP. This condition is met only in the dependent portions of the lung (West zone III), in which pulmonary venous pressure exceeds alveolar pressure; otherwise, PCWP reflects alveolar pressure, not the LAP. Because PEEP decreases the size of West zone III, it has been shown to adversely affect the correlation between the PCWP and LAP, especially in the hypovolemic patient.67–71 Interestingly, acute respiratory distress syndrome (ARDS) seems to prevent the transmission of increased alveolar pressure to the pulmonary interstitium. This preserves the relationship between

900–1400 dynes-sec/cm5 1500–2400 dynes-sec∗m2/cm5

CVP

PAD

PCWP

LAP

LVEDP

LVEDV

150–250 dynes-sec/cm5 250–400 dynes-sec∗m2/cm5

CI = cardiac index; CO = cardiac output; BSA = body surface area; SV = stroke volume; HR = heart rate; MAP = mean arterial pressure; PCWP = pulmonary capillary wedge pressure; PAP = pulmonary arterial pressure; CVP = central venous pressure; SVR = systemic vascular resistance; PVR = pulmonary vascular resistance; SI = stroke index; LVSWI = left ventricular stroke work index; RVSWI = right ventricular stroke work index; SVRI = systemic vascular resistance index; PVRI = pulmonary vascular resistance index. With permission from Reich DL, Mittnacht A, London M, Kaplan JA. Monitoring of the heart and vascular system. In Kaplan JA, Reich DL, Lake CL, Konstadt SL (eds.) Kaplan’s Cardiac Anesthesia 5th ed. Philadelphia: Saunders Elsevier, 2006, pp. 385–436 (table 14-2).

Right ventricle

Pulm. vasc resistance

Airway pressure

Mitral valve

Left ventricular compliance

Figure 7.8. The relationship between the various intracardiac pressure measurements and left ventricular preload. The left ventricular end-diastolic volume (LVEDV) is related to left ventricular end-diastolic pressure (LVEDP) by the left ventricular compliance. The LVEDP is related to the left atrial pressure (LAP) by the diastolic pressure gradient across the mitral valve. The pulmonary capillary wedge pressure (PCWP) is related to the LAP by the pulmonary capillary resistance. The pulmonary artery diastolic pressure (PAD) is an estimate of the PCWP. The central venous pressure (CVP) reflects the PAD if right ventricular function is normal. With permission from Reich DL, Mittnacht A, London M, Kaplan JA. Monitoring of the heart and vascular system. In Kaplan JA, Reich DL, Lake CL, Konstadt SL,eds. Kaplan’s Cardiac Anesthesia, 5th ed. Philadelphia: Saunders Elsevier, 2006, pp. 385–436 (figure 14–11).

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Monitoring in Anesthesia and Perioperative Care

Table 7.4. waveforms

Abnormal central venous and pulmonary artery pressure

Cannon A wave (central venous waveform) Right atrium contracts against closed tricuspid valve r Junctional rhythm r Complete heart block r Ventricular arrhythmias r Ventricular pacing r Tricuspid stenosis Increased resistance to right atrial emptying r Tricuspid stenosis r Right ventricular hypertrophy r Pulmonary stenosis r Pulmonary hypertension V wave (central venous waveform) r Tricuspid regurgitation (early systolic or holosystolic) r Noncompliant right ventricle (late systole) V wave (pulmonary capillary wedge tracing) r Mitral regurgitation r Acute myocardial ischemia r Noncompliant left ventricle

the PCWP and LAP during the application of PEEP.72 In any case, it is not considered prudent to temporarily disconnect patients from PEEP to measure preload.73 The presence of large V waves in the PCWP tracing of patients with mitral regurgitation leads to an overestimation of the LVEDP.74 Table 7.4 lists typical conditions under which cannon A and V waves during central venous and pulmonary artery pressure monitoring are seen. In patients with mitral stenosis, using the PCWP does not provide an accurate estimate of left ventricular filling pressures and may overestimate true preload conditions. Additionally, it has been demonstrated that there is a significant positive gradient between the PCWP and the LAP in the initial hour following CPB.75 Table 7.5 is a summary of conditions that may alter the relationship between the PCWP and the LVEDP.

Evidence of utility CVP monitoring The CVP is a useful monitor if the factors affecting it are recognized and its limitations are understood. The CVP is influenced by the patient’s blood volume, venous tone, and right ventricular performance. However, the complexity of the venous system and right ventricular preload cannot be easily measured or described by measuring right-sided pressures. A true correlation between CVP and left-sided preload is even more difficult to obtain. Mangano showed a good correlation between the CVP and left-sided filling pressures during a change in volume status in patients with coronary artery disease (CAD) and left ventricular ejection fraction (LVEF) greater than 0.4.76 Other studies, however, have not replicated these results, demonstrating weak relationships between the CVP and measures of left ventricular preload.77–80 In general, for clinical purposes, following serial measurements (trends) is more useful than

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Table 7.5. Conditions resulting in discrepancies between pulmonary capillary wedge pressure and left ventricular end-diastolic pressure PCWP ⬎ LVEDP r Positive-pressure ventilation r PEEP r Increased intrathoracic pressure r Non-West lung zone III PAC placement r Chronic obstructive pulmonary disease r Increased pulmonary vascular resistance r Left atrial myxoma r Mitral valve disease (stenosis, regurgitation) PCWP LVEDP r Noncompliant LV (ischemia, hypertrophied LV) r Aortic regurgitation (premature closure of the mitral valve) r LVEDP ⬎ 25 mmHg LVEDP = left ventricular end–diastolic pressure; PCWP = pulmonary capillary wedge pressure; PEEP = positive end–expiratory pressure; PAC = pulmonary artery catheter; LV = left ventricle. Modified from Tuman KJ, Carrol CC, Ivankovich AD. Pitfalls in interpretation of pulmonary artery catheter data. Cardiothorac Vasc Anesth Update 1991;2: 1–24. With permission from: Reich DL, Mittnacht A, London M, Kaplan JA. Monitoring of the heart and vascular system. In Kaplan JA, Reich DL, Lake CL, Konstadt SL, eds. Kaplan’s Cardiac Anesthesia, 5th ed. Philadelphia: Saunders Elsevier, 2006, pp. 385–436 (box 14–6).

looking at individual numbers. Gelman recently published an extensive review of the venous function and central venous pressure.81

PAC monitoring After its introduction in the 1970s, the PAC instantly increased the amount of diagnostic information that could be obtained at the bedside in critically ill patients.82 Information about hemodynamic parameters previously obtainable only in the cardiac catheterization laboratory became readily available to physicians taking care of critically ill patients in various settings. It became obvious that the PAC-derived data provided a more accurate assessment of hemodynamic status and oxygenation when compared with clinical evaluation alone. For example, Connors and coworkers prospectively analyzed 62 consecutive pulmonary artery catheterizations.83 They found that less than half of a group of clinicians correctly predicted the PCWP or cardiac output (CO), and more than 50 percent made at least one change in therapy based on data from the PAC. Waller and associates demonstrated that a group of experienced cardiac anesthesiologists and surgeons who were blinded to the information from the PAC during coronary artery bypass graft (CABG) surgery were unaware of any problem during 65 percent of severe hemodynamic abnormalities.84 Similarly, Iberti and Fisher showed that ICU physicians were unable to accurately predict hemodynamic data on clinical grounds. Sixty percent made at least one change in therapy and 33 percent changed their diagnosis based on PAC data.85 As many as 47 percent of physicians could not correctly determine the PCWP to within 5 mmHg in that study.86

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

However, in the late 1990s, the ability of PACs to positively influence patient outcome came under question. In 1996, Connors and associates87 published the results of a large prospective cohort study. Data were collected from five US teaching hospitals between 1989 and 1994. The researchers enrolled 5735 critically ill adult patients in intensive care settings and surprisingly found that right heart catheterization was associated with an increased mortality in this patient population. The results of this study were instantly criticized and ignited a large number of well-designed studies in the hope of rejecting Connors’ findings. However, the more studies emerged, the more convincing was the evidence that PACs have little impact on patients’ outcome and may actually cause harm.88–93 Various hypotheses are being investigated to explain these findings. Placing a PAC is a highly invasive procedure. Vascular structures are accessed with large-bore introducer sheaths with all possible complications listed below. But most important, even in the best of circumstances, with uncomplicated PAC placement and correct data collection and interpretation, a PAC is a monitoring tool only. As such, we cannot expect a change in patient outcome unless the treatment that is initiated based on our PAC measurements is proven to change patient outcome. In some of the most critically ill patients, such as those with sepsis, ARDS, massive trauma, and so forth, mortality remains high in spite of efforts to find new treatment strategies. Furthermore, diagnoses often can be made on clinical grounds only, and treatment strategies once thought to improve patient outcomes may actually be harmful. The following paragraphs list some of the landmark studies available today regarding PAC use and patient outcomes in various clinical settings. However, major problems with these studies include flaws in study design, and many lack sufficient statistical power. The most common design flaws were a lack of therapeutic protocols or treatment algorithms based on PAC data and inadequate randomization, which introduces observer bias.

Patients undergoing cardiac surgery Nearly all studies looking at patient outcome in cardiac surgery are flawed by lack of adequate randomization and control groups. Furthermore, many retrospective analyses investigate patient populations that underwent cardiac surgery in times when other monitoring tools such as TEE were not as widely used. In spite of this, to date, there are no convincing data showing improved outcome in patients undergoing cardiac surgery with PAC placement compared with central venous pressure monitoring only, and few studies actually suggest that PAC use in patients undergoing low-risk cardiac surgery may even cause harm.94 Schwann and colleagues95 retrospectively assessed the outcome of 2685 patients undergoing coronary artery bypass grafting in whom the decision to place a PAC was based on patient characteristics and risk factors. Using a highly selective strategy, no PAC was used in the majority of cases (91%), and the

outcomes were comparable. In another retrospective trial, Ramsey and associates96 found that pulmonary artery catheterization in elective coronary artery bypass graft surgery was associated with increased in-hospital mortality, longer lengths of stay, and higher total costs. This effect was more pronounced in hospital settings with low overall PAC use. Resano and colleagues looked at PAC use in patients undergoing off-pump coronary artery bypass graft surgery compared with central venous pressure monitoring only and found no difference in outcome.97 In a prospective observational study, Djaiani and coworkers98 looked at 200 consecutive patients undergoing coronary artery bypass surgery when PACs were placed, but the numerical data other than CVP were blinded to the surgeon and anesthesiologist. Patients were managed according to routine, and data could be unblinded if required clinically. Twenty-three percent of patients required unbinding of data; of this 23 percent, preliminary diagnosis was confirmed in 14 percent, and treatment was modified in 9 percent. The patients in the unblinded group went on to experience further morbidity. The researchers thus concluded that placement of a PAC can be safely delayed until the clinical need arises either intraoperatively or in the ICU. Although patients undergoing low-risk cardiac surgery can probably be managed without PAC placement, many clinicians still consider high-risk cardiac surgery and, in particular, patients with right heart failure or pulmonary hypertension as indications for PAC placement. In a prospective, randomized trial, P¨ol¨onen and colleagues applied goal-directed PAC-guided therapy aimed to maintain a mixed venous saturation = 70 percent and blood lactate ⬍ 2 mmol/L in patients following cardiac surgery. Using this strategy, they found that increasing oxygen delivery in the immediate postoperative period shortened hospital stay and decreased morbidity.99

Patients undergoing major noncardiac surgery Major noncardiac surgery is composed of a very diverse group of surgeries, including cases in which hemodynamic instability is often anticipated. Examples are trauma, major vascular, abdominal, and thoracic surgeries, including liver resections and transplantations. The differential diagnosis of sudden perioperative hemodynamic decompensation is complicated by numerous comorbidities that are often present in these patient populations. Nevertheless, there are no conclusive data that any patient population undergoing major noncardiac surgery may benefit from PAC monitoring. Some studies even suggest adverse outcomes related to PAC use. In 2001, Polanczyk and coworkers100 published the results of an observational study on 4059 patients undergoing major elective noncardiac procedures, looking at the relationship between pulmonary artery catheterization and postoperative cardiac complications. The use of a PAC was associated with an increased incidence of major postoperative cardiac events. Sandham and associates101 reported a prospective, randomized, controlled outcome study of 1994 high-risk patients (ASA III

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or IV) scheduled for major noncardiac surgery followed by ICU stay, who were managed with or without the use of a PAC. No benefit in goal-directed therapy with the use of PAC data as compared with standard care (without the use of PAC) was found. Furthermore, they found a higher risk of pulmonary embolism in the PAC group.

Critically ill patients in ICU settings The trend toward decreasing the use of the PACs continues and includes patients admitted to an ICU setting. The most significant decrease in PAC use has been documented in patients with acute myocardial infarction, whereas patients diagnosed with septicemia show the least decline in PAC use.102 Admissions to an ICU typically represent a diverse group of critically ill, multimorbid, and/or high-risk patients prone to adverse events. Nevertheless, to date, there are no data from any large, well-designed, prospective studies showing that PAC placement improves outcome in any of the major clinical ICU diagnoses. Yu and associates103 performed a prospective cohort study of the relationship between PAC use and outcome in 1010 patients with severe sepsis. PAC monitoring did not improve outcome in this patient population. Sakr and colleagues looked at outcome related to PAC use in 3147 adult patients admitted to an ICU, a subanalysis of a large multicenter prospective observational study designed to evaluate the epidemiology of sepsis in European countries.104 After propensity score matching, there was no significant difference in outcome with or without PAC placement. Interestingly, significant differences in PAC use were reported between the various participating countries. A prospective randomized study by Rhodes and coworkers105 found no significant difference in mortality in critically ill patients treated with or without the use of a PAC. Adjusting for the severity of illness, Murdoch and colleagues106 found that the use of the PAC in patients in the ICU is safe, but no benefit was demonstrated. Chittock and associates107 demonstrated that severity of illness may play an important role in defining subgroups of patients who may benefit from PAC monitoring. Of 7310 critically ill adult patients admitted to the ICU, those with APACHE II scores ⬎31 showed decreased mortality with PAC monitoring, whereas patients with lower APACHE II scores had increased mortality. The PAC-Man study, a randomized controlled trial, enrolled 1041 patients from 65 ICUs throughout the United Kingdom. Patients were randomly assigned to management with or without PAC placement. Treatment in both arms of the study was at the discretion of the treating clinician. Neither benefit nor harm related to PAC use was found. This study has been criticized for lack of a standardized treatment protocol based on PAC data, which is a major design flaw in many otherwise well-randomized prospective studies. The ESCAPE trial (Evaluation Study of Congestive Heart Failure and PAC Effectiveness) looked at patients with symptoms of severe heart failure. This multicenter, randomized,

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controlled trial enrolled 433 patients at 26 sites. Again, there was no specific treatment protocol to follow. However, the use of inotropes was discouraged, and investigators were asked to follow national guidelines for treatment of heart failure, which promote the use of diuretics and vasodilators. The target in both groups was improvement of clinical symptoms of heart failure. In the PAC group there was an additional target of a pulmonary capillary occlusion pressure of 15 mmHg and a right atrial pressure of 8 mmHg. Overall mortality did not differ between the two groups; however, more adverse events were recorded in the PAC group. Exercise and quality-of-life measures improved in both groups, and the investigators reported a trend toward greater improvement with PAC use. These findings have been reproduced similarly in patients with ARDS. Two randomized controlled studies could not show improved patient outcome with PAC use.108,109 Randomized trials including patients with acute myocardial infarction seemed to also confirm these data.110,111 Cohen and colleagues112 retrospectively studied 26,437 patients with acute coronary syndromes. A PAC catheter was inserted in 2.8 percent of patients. Patients in the United States were 3.8 times more likely to have a PAC placed than were non-US patients. After adjustment for confounding factors, PAC use was associated with a 2.6-fold increase in hospital mortality. The subset of patients who developed cardiogenic shock had similar outcomes both with and without PAC use. Haupt and coworkers suggested that patients in the ICU might have disease too far advanced to make invasive hemodynamic monitoring useful.113 Some of the earlier studies that had reported improved outcome used invasive hemodynamic monitoring to optimize oxygen delivery in the perioperative period.114–117 In a meta– analysis, Heyland and associates argued similarly that “maximizing oxygen delivery” in the perioperative setting (i.e. prior to the onset of irreversible organ damage) is more effective in comparison with doing so in the chronic ICU setting.118 The previous discussion illustrated examples of the broad spectrum of critically ill patient populations, and the clinical settings in which PACs have been frequently deployed. The findings regarding patient outcome discussed previously and available in the literature have led to a dramatic decrease in PAC use in many clinical settings. In the 1990s, as TEE began to gain popularity and concern grew as to the risks of PA catheters, there was a significant drop in the use of PACs. A time trend analysis looked at PAC use over 10 years, from 1993 to 2004, and showed a 63 percent decrease in use, which was evident in both cardiac and noncardiac surgical admissions.119 Wiener and colleagues point out that the decline began in 1994, likely owing to the fact that preliminary data from the Connors group were presented at the American Thoracic Society conference and that early adopters may have stopped placing PACs. However, the largest step-off in use occurred in 1996, likely correlating with the actual publication of the Connors study. Ranucci looked at the PAC and its relationship with TEE.120 He purported that the information sets gained from each technology are not interchangeable but rather complementary to one another. This may

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

explain why, although TEE is becoming more readily available, PAC has not fallen completely out of favor. Most practitioners taking care of critically ill patients still value PAC as an important monitoring tool. There are some data showing that small subgroups of patients may benefit from PAC use, and there is enough evidence to prove that if deployed carefully, there is minimal risk with PAC use. It is the opinion of the authors of this text that the PAC still has a role in modern evidence-driven medicine. The risks associated with perioperative PAC monitoring may outweigh the benefits in low-tomoderate–risk patients, whereas high-risk patients undergoing major surgery probably benefit from right heart catheterization. Specific situations in which PAC use may be useful are discussed later in this chapter.

Complications CVP The complications of central venous cannulation can be divided roughly into three categories: complications of vascular access, complications of catheter insertion, or complications of catheter presence. These are summarized in Table 7.6. Specific information regarding several of the complications is detailed below. Inadvertent arterial puncture during central venous cannulation is not uncommon.121 The two main reasons that this phenomenon occurs are that all veins commonly used for cannulation lie in close proximity to arteries (except the EJV and cephalic vein), and that the venous anatomy is quite variable. Localized hematoma formation is the usual consequence. This may be minimized if a small-gauge needle is initially used to localize the vein122 or ultrasonic guidance is employed (see previous discussion). If arterial puncture occurs with a large-gauge needle or catheter, direct pressure may be difficult to apply owing to the location of the artery. If the patient has a coagulopathy, a massive hematoma may form. In the neck, this may lead to airway obstruction, requiring urgent tracheal intubation. In the arm or leg, venous obstruction may occur. If the artery is cannulated with a large-bore catheter, a surgical consultation may be required before its removal. Reports about successful Table 7.6. r r r r r r r r r r r r r r

Complications of central venous cannulation

Arterial puncture with hematoma Arteriovenous fistula Hemothorax Chylothorax Pneumothorax Nerve injuries (e.g. brachial plexus) Stellate ganglion injury (Horner syndrome) Air embolization Catheter or wire shearing Right atrial or right ventricular perforation Thrombosis, thromboembolism Infection, sepsis, endocarditis Arrhythmias Hydrothorax

percutaneous repair of inadvertent arterial injuries following central venous cannulation have been published.123,124 Arteriovenous fistula from the carotid artery to the IJV has also been reported following central venous cannulation.125,126 Hemothorax may occur if the subclavian artery is lacerated during cannulation attempts. Symptoms of hypovolemia may predominate because of the large capacity of the pleural cavity.127 Injury to the thoracic duct resulting in chylothorax has been reported following left IJV and left subclavian vein cannulation.128,129 This is a serious complication that may require surgical treatment.130 Fear of this complication is one of the main reasons for selecting right-sided IJV and subclavian approaches for central venous cannulation. If the pleural cavity is entered and lung tissue is punctured during an attempt at cannulation, a pneumothorax may result. Tension pneumothorax is possible if air continues to accumulate in the pleural space as a result of a “ball-valve” effect. Pneumothorax is most common with subclavian punctures and occurs only rarely with IJV cannulation.131,132 The brachial plexus, stellate ganglion, and phrenic nerve all lie in close proximity to the IJV. These structures may be injured during cannulation attempts. Paresthesias of the brachial plexus are not uncommon during attempts to localize the IJV. Direct needle trauma is the most likely cause of paresthesias or motor deficits; this risk is somewhat increased by the long-beveled needles used for vascular access.133,134 Transient deficits may result from the deposition of local anesthetic in the brachial plexus, stellate ganglion, or cervical plexus. A large hematoma or pseudoaneurysm could result in nerve injury after an inadvertent arterial puncture.135,136 Horner’s syndrome has also been reported following IJV cannulation.137 Venous air embolism is a potentially fatal complication that can occur in situations in which there is negative pressure in the venous system. There is a risk of paradoxical embolization in patients with a patent foramen ovale or other intracardiac defects, such as an atrial or ventricular septal defect. During central venous cannulation, air embolism can usually be prevented with positional maneuvers, such as the Trendelenburg position, which increases the venous pressure in the vessel. After the CVP catheter has been placed, it is important to ensure that the catheter is firmly attached to its connecting tubing. Air embolism may occur even after the catheter has been removed if the subcutaneous tract persists.138 The diagnosis of venous air embolism is likely when there is a sudden onset of tachycardia associated with pulmonary hypertension and systemic hypotension. A new murmur may be heard owing to turbulent flow in the RV outflow tract. Twodimensional echocardiography (transesophageal or transthoracic) and precordial Doppler probe monitoring are highly sensitive methods of detecting air embolism. Venous air embolism is most effectively treated by aspirating the air via a catheter positioned at the SVC–RA junction. Catheter or guidewire fragments may be sheared off by the inserting needle and may embolize to the right heart and pulmonary circulation when either catheter-through-needle or

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Seldinger-type cannulation kits are used. It is also possible to lose a guidewire within the patient by not withdrawing a sufficient length of the wire to grasp it at the external end prior to inserting the catheter.139 The catheter fragment position within the right-sided circulation will determine whether surgery or percutaneous transvenous techniques are necessary for its removal.140 These complications can almost always be avoided by using proper technique. A catheter must never be withdrawn through the inserting needle. Reinsertion of needles into standard (catheter-over-needle) intravenous cannulae is not recommended but should certainly never be performed if the cannula is kinked or resistance is encountered. Similarly, guidewires should not be inserted through cannulae if blood return is not present, or forcefully inserted if resistance is encountered. Additionally, guidewires should not be withdrawn through inserting needles. During unsuccessful catheterization, the needle and catheter, or needle and guidewire, must be withdrawn simultaneously. If the RA or RV is perforated during central venous cannulation, pericardial effusion or tamponade may result and the patient may require surgical treatment.141 The likelihood of this complication is increased with the use of inflexible guidewires, long dilators, or long catheters. This complication has also been reported with the use of an indwelling polyethylene catheter.142 Oropello and colleagues suggested that the dilators used in many of the central catheters kits may be a major cause of vessel perforation.143 They believe that the dilator may bend the guidewire, creating its own path, thus causing it to perforate a vessel wall. In addition, it was noted that a number of kits have dilators that are much longer than the catheters and present a further risk factor for possible perforation of the heart or vessels. Kinking of the guidewire in large-bore introducer kits can be prevented by guidance of the introducer or catheter distally close to the patient’s skin. If the catheter tip is placed extravascularly in the pleural cavity or erodes into this position, the fluid that is infused into the catheter will accumulate in the pleural cavity, causing hemoor hydrothorax. A pleurocentesis or thoracostomy (chest) tube might be necessary and surgical consultation may be required. Transient atrial and/or ventricular arrhythmias commonly occur as the guidewire is passed into the RA or RV during central venous cannulation using the Seldinger technique. This most likely results from the relatively inflexible guidewire causing extrasystoles as it contacts the endocardium. Ventricular fibrillation during guidewire insertion has been reported.144 There are also reports of complete heart block from guidewire insertion during central venous cannulation.145 These cases can be managed successfully using a temporary transvenous or external pacemaker. The problem most likely results from excessive insertion of the guidewire, with irritation of the right bundle branch. It is recommended that, to prevent these complications, the length of guidewire insertion be limited to the length necessary to reach the SVC–RA junction. It is also imperative to monitor the patient appropriately (i.e.

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ECG and/or pulse monitoring) and to have resuscitative drugs and equipment immediately available when performing central venous catheterization. Strict aseptic technique is required to minimize catheterrelated bloodstream infections. Full-barrier precautions during insertion of central venous catheters have been shown to decrease the incidence of catheter-related infections.146,147 Subcutaneous tunneling of catheters inserted into the internal jugular and femoral veins,148,149 antiseptic-barrier–protected catheter hubs,150 and antiseptic/antibiotic-impregnated shortterm catheters151,152 have also been shown to reduce catheter– related infections.153 There is accumulating evidence that 2% chlorhexidine preparation for skin antisepsis is associated with a reduced risk of catheter-related infections.154–156 Hospital policies differ with respect to the permissible duration of catheterization at particular sites, but routine replacement of central venous catheters to prevent catheter-related infections is not recommended.157,158

PAC The complications associated with PAC placement inherently include almost all those detailed in the section on CVP placement (see previous section). Additional complications that are unique to the PAC are detailed here (also see Table 7.7) The ASA Task Force on Pulmonary Artery Catheterization concluded that serious complications resulting from PAC catheterization occur in 0.1 percent to 0.5 percent of patients monitored with a PAC.199 Higher estimates are found in the literature and probably represent different patient populations, hospital settings, level of experience with PAC management, and other factors.159 The most common complications associated with PAC insertion are transient arrhythmias, especially premature ventricular contractions (PVCs).160 However, fatal arrhythmias have rarely been reported.161,162 Positioning the patient in slight reverse Trendelenburg position and right lateral tilt can help prevent arrhythmias during PAC insertion (compared with the Trendelenburg position). Complete heart block may develop during PA catheterization in patients with preexisting left bundle-branch block (LBBB).163–165 This potentially fatal complication is most likely the result of electrical irritability from the PAC tip, causing a transient right bundle-branch block (RBBB) as it passes through the right ventricular outflow tract. The incidence of Table 7.7. r r r r r r r

Pulmonary artery specific complications

Transient dysrhythmias Right bundle-branch block Complete heart block (in patients with existing left-bundle branch block) Pulmonary artery rupture Pulmonary infarction Pulmonary artery knotting Tricuspid valve and subvalvular damage

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

developing RBBB was 3 percent in a prospective series of patients undergoing PA catheterization.166 However, none of the patients with preexisting LBBB developed complete heart block in that series. In another study of 47 patients with LBBB, there were two cases of complete heart block, but only in patients with recent onset of LBBB.167 It is imperative to have an external pacemaker immediately available or to use a pacing PAC when placing a PAC in patients with LBBB. Hannan and associates reported a 46 percent mortality rate in a review of 28 cases of PAC-induced endobronchial hemorrhage, but the mortality rate was 75 percent in anticoagulated patients.168 From these reports, several risk factors have emerged: advanced age, female sex, pulmonary hypertension, mitral stenosis, coagulopathy, distal placement of the catheter tip, and balloon hyperinflation. Balloon inflation in distal PAs is probably accountable for most episodes of PA rupture, owing to the high pressures generated by the balloon.169 Hypothermic cardiopulmonary bypass (CPB) may also increase risk because of the distal migration of the catheter tip with movement of the heart and hardening of the PAC.170,171 It is common practice to pull the PAC back approximately 3 to 5 cm when CPB is instituted. It is important to consider the etiology of the hemorrhage when formulating a therapeutic plan. If the hemorrhage is minimal, and a coagulopathy coexists, correction of the coagulopathy may be the only necessary therapy. Protection of the uninvolved lung is of prime importance. Tilting the patient toward the affected side, and isolation of the lungs by placement of a double-lumen endotracheal tube or bronchial blocker, should protect the contralateral lung.172 Strategies proposed to stop the hemorrhage include the application of PEEP, placement of bronchial blockers, and pulmonary resection.173,174 The clinician is obviously at a disadvantage unless the site of hemorrhage is known. A chest radiograph will usually indicate the general location of the lesion. Although the etiology of endobronchial hemorrhage may be unclear, the bleeding site must be unequivocally located before surgical treatment is attempted. Using fluoroscopy and a small amount of radiographic contrast dye may help pinpoint the lesion if active hemorrhage is present. In severe hemorrhage and with recurrent bleeding, transcatheter coil embolization has been used. This may emerge as the preferred treatment method.175,176 Pulmonary infarction is a rare complication of PAC monitoring. An early report suggested that there was a 7.2 percent incidence of pulmonary infarction with PAC use.177 However, continuously monitoring the PA waveform and keeping the balloon deflated when not determining the PCWP (to prevent inadvertent wedging of the catheter) were not standard practice at that time. Distal migration of PACs may also occur intraoperatively because of the action of the RV, uncoiling of the catheter, and softening of the catheter over time. Inadvertent catheter wedging occurs during CPB because of the diminished RV chamber size and retraction of the heart to perform the operation. Embolization of thrombus formed on a PAC could also result in pulmonary infarction.

Knotting of a PAC usually occurs as a result of coiling of the catheter within the right ventricle.178 Insertion of an appropriately sized guidewire under fluoroscopic guidance may aid in unknotting the catheter.179 Alternatively, the knot may be tightened and withdrawn percutaneously along with the introducer if no intracardiac structures are entangled.180,181 If cardiac structures, such as the papillary muscles, are entangled in the knotted catheter, or if the knot appears too large, then surgical intervention may be required.182–184 Sutures placed in the heart may inadvertently entrap the PAC. A report of such a case and the details of the percutaneous removal have been described.185 Placement of a PAC may cause or increase tricuspid regurgitation just by its physical presence in the right heart.186 Additionally, withdrawal of the catheter with the balloon inflated may result in injury to the tricuspid187 or pulmonary valves.188 Placement of the PAC with the balloon deflated may increase the risk of passing the catheter between the chordae tendinae.189 Septic endocarditis has also resulted from an indwelling PAC.190,191 The PAC is a foreign body that may serve as a nidus for thrombus formation. Mild thrombocytopenia has been reported in dogs and humans with indwelling PACs.192 This probably results from increased platelet consumption. Heparinbonded PACs reduce thrombogenicity for up to 72 hours.193,194 However, heparin-coated PACs might trigger heparin-induced thrombocytopenia (HIT).195 The catheter may pass through an interatrial or interventricular communication into the left side of the heart. It is then possible for the catheter to enter the aorta through the left ventricular outflow tract. This complication should be recognized by the similarity between the presumed PA and systemic arterial waveforms. Placement of the PAC in the liver has also been described, and the wedged hepatic venous pressures may mimic the PA pressure waveform.196 Again, if available, TEE has proved invaluable for real-time confirmation of the proper placement of PACs. In many case reports, TEE detected incorrect placement and complications resulting from PACs. Balloon rupture is not uncommon when the PAC has been left in place for several days or when the balloon is inflated with more than 1.5 mL of air. Small volumes of air injected into the PA are of little consequence, and balloon rupture is apparent if the injected air cannot be withdrawn. Right ventricular perforation is an especially rare complication with a balloon-tipped catheter but has been reported in the literature.197 Malfunctions of the catheter and balloon can lead to inaccurate PCWP waveforms and data leading to incorrect treatment of the patient. Shin and coworkers reported a problem of eccentric balloon inflation, causing the catheter tip to impinge on the PA wall.198 Catheter whip is an artifact that is associated with long catheters, such as PACs. Because the tip moves within the bloodstream of the cardiac chambers and great vessels, the fluid contained within the catheter is accelerated. This can produce superimposed pressure waves of 10 mmHg in either direction.

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Credentialing Currently there are no recommendations for training and credentialing processes regarding PAC monitoring. However, the 2003 ASA guidelines for pulmonary artery catheterization emphasize that patient, surgery, and practice setting must be considered.199 The ASA Task Force concluded that the practice setting, among other factors, is important, as there is evidence that inadequate training or experience may increase the risk of perioperative complications associated with the use of PACs. Thus, it is recommended that the routine use of PACs should be confined to centers with adequate training and experience in the perioperative management of patients with PACs. Residents enrolled in an Accreditation Council for Graduate Medical Education (ACGME)–accredited residency program are required to have experience with “patients who require specialized techniques for their perioperative care . . . [and] significant experience with central vein and pulmonary artery catheter placement.” Interestingly, there are no specific requirements for ACGME-accredited cardiothoracic anesthesiology fellowship programs with regard to PACs. As previously discussed, the use of PACs has been declining significantly as data have emerged questioning their benefit in patient outcome. This then leads to less training and experience in the use PACs. The impact of decreased exposure to PACs may lead to increasing complications secondary to inexperience and operator error.

Practice parameters (indications) Indications for CVP monitoring CVP monitoring is often performed to obtain an indication of intravascular volume status. However, the accuracy and reliability of CVP monitoring depend on many factors, including the functional status of the RV and LV, the presence of pulmonary disease, and ventilatory factors, such as PEEP. The CVP may reflect left heart filling pressures, but only in patients with good LV function. Patients undergoing cardiac surgery with CPB should have the CVP monitored. When the catheter tip is positioned in the SVC, it indicates both RA pressure and cerebral venous pressure. Significant increases in CVP can produce critical decreases in cerebral perfusion pressure. During CPB, this is occasionally caused by a malpositioned SVC cannula, resulting in decreased venous drainage to the CPB machine. The surgeon must correct it immediately to prevent cerebral edema and poor cerebral perfusion. Aside from patient- and surgery-related factors, indications for CVP monitoring may also depend on practice setting and on the preferences of the surgeon and anesthesiologist. If a central venous catheter is used only for volume access, it should be kept in mind that shorter large-bore peripheral lines allow higher flow rates than the longer central line catheters. Table 7.8 summarizes some of the indications for the perioperative use of a central venous catheter.

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Table 7.8. Indications and contarindications for central venous catheter placement

Indications r Major operative procedures involving large fluid shifts and/or blood loss r Inadequate peripheral venous access r Frequent venous blood sampling r Rapid infusion of intravenous fluids (e.g. major trauma, liver transplantation) r Venous access for vasoactive or irritating drugs r Chronic drug administration (e.g. antibiotics, chemotherapy) r Total parenteral nutrition r Surgical procedures with a high risk of air embolism r Intravascular volume assessment when urine output is not reliable or unavailable (e.g. renal failure) Contraindications r SVC syndrome r Skin infection at insertion site

Contraindications for CVP monitoring There are few absolute contraindications for CVP monitoring. In patients with true SVC syndrome, placement of a CVP in the neck, subclavian area, or the upper extremities is contraindicated. Venous pressures in the head and upper extremities are elevated by the SVC obstruction, and therefore do not reflect RA pressure. Medications that are administered into the obstructed venous circulation reach the central circulation via collateral vessels in a delayed fashion. Furthermore, rapid fluid administration into the obstructed venous circulation may exacerbate the elevated venous pressures and cause more pronounced edema. The mild SVC obstruction seen with some ascending aortic aneurysms, however, does not represent a contraindication to central venous cannulation of the upper body. An infection at the side of insertion is another absolute contraindication. In coagulopathic patients, ultrasoundguided central line placement is preferred to reduce the risk of arterial puncture and subsequent hematoma formation in the neck.

Indications for PAC placement The ability of PACs to positively influence patient outcome has never been conclusively proved in large-scale prospective studies (see previous discussion). To the contrary, enough evidence has been collected to seriously question the indiscriminate use of PA catheters. In general, the risk–benefit ratio of PAC placement should be evaluated for each individual case, rather than based on broad recommendations.200,201 In 2003, the ASA Task Force on Pulmonary Artery Catheterization published updated practice guidelines for pulmonary artery catheterization (http://www.asahq.org/publicationsAndServices/pulm artery.pdf).These guidelines emphasized that the combination of patient, surgery, and practice setting had to be considered. Generally, the routine use of PACs is indicated in highrisk patients (e.g. ASA 4 or 5) and high-risk procedures (e.g. where large fluid changes or hemodynamic disturbances are

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

Table 7.9.

ASA practice guidelines for pulmonary artery catheter use

Opinions r PA catheterization provides new information that may change therapy r r r

r r r

with poor clinical evidence of its effect on clinical outcome or mortality. There is no evidence from large controlled studies to date that preoperative PA catheterization improves outcome regarding hemodynamic optimization. Perioperative PAC monitoring of hemodynamic parameters leading to goal-directed therapy has produced inconsistent data in multiple studies as well as clinical scenarios. Having immediate access to PA catheter data allows important preemptive measures for selected subgroups of patients who encounter hemodynamic disturbances that require immediate and precise decisions about fluid management and drug treatment. Experience and understanding are the major determinants of PA catheter effectiveness. PA catheterization is inappropriate as a routine practice in surgical patients and should be limited to cases in which the anticipated benefits of catheterization outweighs the potential risks. PA catheterization can be harmful.

Recommendations r The appropriateness of routine PA catheterization depends on a r

r

r

r

combination of patient-, surgery-, and practice setting-related factors. Perioperative PA catheterization should be considered in patients who present with significant organ dysfunction or major comorbidity that poses an increased risk for hemodynamic disturbances or instability (e.g. ASA 4 or 5 patients). Perioperative PA catheterization in surgical settings should be considered based on the hemodynamic risk of the individual case rather than generalized surgical setting related recommendations. High-risk surgical procedures are those where large fluid changes or hemodynamic disturbances can be anticipated and procedures that are associated with a high risk of morbidity and mortality. Because of the risk of complication from PA catheterization, the procedure should not be performed by clinicians, nursing staff, or in practice settings where competency in safe insertion, accurate interpretation of results, and appropriate catheter maintenance cannot be guaranteed. Routine PA catheterization is not recommended when the patient, procedure, and practice setting each pose a low- or moderate- risk for hemodynamic changes.

ASA = American Society of Anesthesiologists; PA = pulmonary artery. American Society of Anesthesiologists: Practice guidelines for pulmonary artery catheterization: http://www.asahq.org/publicationsAndServices/ pulm_artery.pdf.

expected). The practice setting is important, as there is evidence that inadequate training or experience may increase the risk of perioperative complications associated with the use of PAC. Thus, it is recommended that the routine use of PAC should be confined to centers with adequate training and experience in the perioperative management of patients with PACs. The ASA guidelines specifically do not provide the practitioner with a list of procedures or diagnoses for which PAC placement is indicated (also see Table 7.9). Considering the bulk of literature showing no benefit, or even worse outcome, if PAC was deployed, even in patients with severely compromised cardiac function, the authors of this text also conclude that there are

Table 7.10.

Contraindications for pulmonary artery catheterization

Absolute contraindications r Right atrial or right ventricular mass r Tricuspid or pulmonary stenosis r Mechanical tricuspid or pulmonary valve prosthesis Relative contraindications r Recently placed pacemaker or defibrillator wires r Patients with left bundle-branch block

very few, if any, clearly defined indications for PAC monitoring left in today’s practice. Even though there are no evidencebased data to support this, it is our opinion that patients with known or suspected pulmonary hypertension can benefit from PAC placement. Significant expertise and training are required for PAC placement as well as for interpretation of PAC-derived data. Many anesthesiology residency training programs, as well as cardiothoracic surgery and intensive care fellowship programs, place PACs more frequently, to provide adequate training. Lack of exposure to PACs could otherwise lead to inadequate expertise among these physicians and potentially increase the risk of complications related to PAC placement.

Contraindications to PAC placement A list of contraindications to PAC placement is provided in Table 7.10. A right atrial or right ventricular mass (tumor or thrombus) is considered an absolute contraindication to PAC placement. The catheter may dislodge a portion of the mass, causing pulmonary or paradoxical embolization. In patients with tricuspid or pulmonic valvular stenosis, PAC placement should be considered carefully, as it may be difficult or impossible to pass a PAC across a severely stenotic valve and, in fact, it may worsen the obstruction to flow. Patients with certain valvular diseases, such as significant mitral and aortic stenosis, are sensitive to even brief periods of arrhythmias. Brief periods of atrial and ventricular arrhythmias can be seen during PAC placement in the majority of cases and could potentially cause acute hemodynamic instability. Appropriate preparations must be made to enable rapid administration of antiarrhythmic drugs and cardiopulmonary resuscitation, and electrical cardioversion, defibrillation, or pacing if required. In coagulopathic patients PAC is not generally contraindicated; however, increased precautions should be taken to prevent hematoma formation, as mentioned previously. Additionally, the risk of inducing endobronchial hemorrhage may be increased. Newly inserted pacemaker wires may be displaced by the catheter during insertion or withdrawal. After approximately four to six weeks, pacemaker wires become firmly embedded in the endocardium, and wire displacement becomes less likely. Newer generation pacemaker and defibrillator wires are now anchored into the endocardium more securely during placement and are less likely to become dislodged.

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Specialty catheters Pacing catheters Electrode PACs, as well as pacing wire catheters, are available. Electrode PACs (Swan-Ganz Pacing PAC, originally produced by Baxter Edwards) contain five electrodes for bipolar atrial, ventricular, or AV sequential pacing. With appropriate filtering, the catheter may also be used for the recording of an intracardiac ECG. The intraoperative success rates for atrial, ventricular, and AV sequential capture have been reported as 80 percent, 93 percent, and 73 percent, respectively.202 The Paceport and A-V Paceport catheters (Baxter Edwards) have lumina for the introduction of a ventricular wire (Paceport), or both atrial and ventricular wires (A-V Paceport) for temporary transvenous pacing. The success rate for ventricular pacing capture was 96 percent for the Paceport.203 The success rates for atrial and ventricular pacing capture prior to CPB were 98 percent and 100 percent, respectively, in a study of the A-V Paceport.204 The actual use and indications for placement of pacing PAC in a series of cardiac surgery patients has been published.205 The possible indications for placement of a pacing PAC are shown in Table 7.11.

Right ventricular ejection fraction catheters The rapid-response thermistor PAC (Baxter Edwards) incorporates three modifications from a standard PAC: a multiorifice injectate port; a rapid-response thermistor; and ECG electrodes. The catheter is positioned so the injectate port is 2 cm cephalad to the tricuspid valve in the RA.206,207 With each injection, the computer determines the right ventricular ejection fraction (RVEF) from the exponential decay of the thermodilution curve. End-diastolic temperature points in the thermodilution curve are identified using the R-wave signal. The computer also measures heart rate (HR) from the catheter ECG electrodes. From these data, stroke volume (SV), right ventricular end-diastolic volume, and right ventricular end-systolic volume are calculated. Assumptions that are essential to the accuracy of the technique include a regular RR interval, instantaneous mixing of the injectate with the RV blood, and absence of tricuspid regurgitation. The timing of injection with respect to the respiratory cycle also affects the reproducibility of the Table 7.11. Potential indications for the perioperative placement of pacing pulmonary artery catheters r r r r r r r r r

Sinus node dysfunction/bradycardia Second-degree (Mobitz II) atrioventricular block Complete (third-degree) atrioventricular block Digitalis toxicity Need for AV sequential pacing Aortic stenosis (need to maintain sinus rhythm) Severe left ventricular hypertrophy or noncompliant left ventricle HCM (obstructive type) Need for an intracardiac electrogram

HCM = hypertrophic cardiomyopathy

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measurements.208 The use of this type of monitoring could be justified in patients with severe RV dysfunction caused by myocardial infarction, right-sided CAD, pulmonary hypertension, left-sided failure, or intrinsic pulmonary disease. However, RVEF catheters are rarely used, especially with TEE becoming more readily available in the OR setting.

Mixed venous oxygen saturation catheters The addition of fiberoptic bundles to PACs has enabled the continuous monitoring of venous oxygen saturation (SvO2 ) using reflectance spectrophotometry. The catheter is connected to a device that includes a light-emitting diode and a sensor to detect the light returning from the PA. SvO2 is calculated from the differential absorption of various wavelengths of light by the saturated and unsaturated hemoglobin.209 Monitoring the SvO2 is a means of providing a global estimation of the adequacy of oxygen delivery relative to oxygen extraction rate. The formula for SvO2 calculation can be derived by modifying the Fick equation and assuming that the effect of dissolved oxygen in the blood is negligible: SvO2 = SaO2 −

V˙ O2 C O • 1.34 • Hb

A decrease in the SvO2 can indicate one of the following situations: (1) decreased CO; (2) increased oxygen consumption; (3) decreased arterial oxygen saturation; or (4) decreased hemoglobin concentration (also see the following chapter). If it is assumed that oxygen consumption and arterial oxygen content are constant, then changes in SvO2 should reflect changes in CO. The values obtained with various fiberoptic catheter systems showed good agreement with in vitro (co-oximetry) SvO2 measurements.210–213

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Chapter 7 – Central Venous and Pulmonary Artery Catheterization

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117. Moore CH, Lombardo TR, Allums JA, Gordon FT. Left main coronary artery stenosis: Hemodynamic monitoring to reduce mortality. Ann Thorac Surg 1978;26:445–51. 118. Heyland DK, Cook DL, King D, et al. Maximizing oxygen delivery in critically ill patients: A methodologic appraisal of the evidence. Crit Care Med 1996;24:517–24. 119. Wiener RS, Welch HG. Trends in use of the pulmonary artery catheter in the United States, 1993–2004. JAMA 2007;298:423–9. 120. Ranucci M. Which cardiac surgical patients can benefit from placement of a pulmonary artery catheter? Crit Care 2006;10(Suppl3):S6. 121. Applebaum RM, Adelman MA, Kanschuger MS, et al. Transesophageal echocardiographic identification of a retrograde dissection of the ascending aorta caused by inadvertent cannulation of the common carotid artery. J Am Soc Echocardiogr 1997;10:749–51. 122. Eckhardt W, Iaconetti D, Kwon J, et al. Inadvertent carotid artery cannulation during pulmonary artery catheter insertion. J Cardiothorac Vasc Anesth 1996;10:283–90. 123. Fraizer MC, Chu WW, Gudjonsson T, Wolff MR. Use of a percutaneous vascular suture device for closure of an inadvertent subclavian artery puncture. Catheter Cardiovasc Interv 2003;59:369–71. 124. Berlet MH, Steffen D, Shaughness G, Hanner J. Closure using a surgical closure device of inadvertent subclavian artery punctures during central venous catheter placement. Cardiovasc Intervent Radiol 2001;24:122–4. 125. Gobiel F, Couture P, Girard D, et al. Carotid artery-internal jugular fistula: Another complication following pulmonary artery catheterization via the internal jugular venous route. Anesthesiology 1994;80:230–1. 126. Robinson R, Errett L. Arteriovenous fistula following percutaneous internal jugular vein cannulation: A report of carotid artery-to-internal jugular vein fistula. J Cardiothorac Anesth 1988;2:488–91. 127. Kim J, Ahn W, Bahk JH. Hemomediastinum resulting from subclavian artery laceration during internal jugular catheterization. Anesth Analg 2003;97:1257–9. 128. Kwon SS, Falk A, Mitty HA. Thoracic duct injury associated with left internal jugular vein catheterization: anatomic considerations. J Vasc Interv Radiol 2002; 13:337–9. 129. Khalil DG, Parker FB, Mukherjee N, Webb WR. Thoracic duct injury: a complication of jugular vein catheterization. JAMA 1972;221:908–9. 130. Teba L, Dedhia HV, Bowen R, Alexander JC. Chylothorax review. Crit Care Med 1985;13:49–52. 131. Cook TL, Deuker CW. Tension pneumothorax following internal jugular cannulation and general anesthesia. Anesthesiology 1976;45:554–5. 132. Plewa MC, Ledrick D, Sferra JJ. Delayed tension pneumothorax complicating central venous catheterization and positive-pressure ventilation. Am J Emerg 1995;Med 13:532–5. 133. Porzionato A, Montisci M, Manani G. Brachial plexus injury following subclavian vein catheterization: a case report. J Clin Anesth 2003;15:582–6. 134. Selander D, Dhuner K-G, Lundborg G. Peripheral nerve injury due to injection needles used for regional anesthesia. An experimental study of the acute effects of needle point trauma. Acta Anaesth Scand 1977;21:182. 135. Karakaya d, Baris S, Guldogus F, et al. Brachial plexus injury during subclavian vein catheterization for hemodialysis. J Clin Anesth 2000;12:220–3.

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136. Nakayama M, Fulita S, Kawamata M, et al. Traumatic aneurysm of the internal jugular vein causing vagal nerve palsy: a rare complication of percutaneous catheterization. Anesth Analg 1994;78:598–600. 137. Parikh RD. Horner’s syndrome: a complication of percutaneous catheterization of the internal jugular vein. Anaesthesia 1972;27:327–9. 138. Turnage WS, Harper JV. Venous air embolism occurring after removal of a central venous catheter. Anesth Analg 1991;72:559–60. 139. Akazawa S, Nakaigawa Y, Hotta K. Unrecognized migration of an entire guidewire on insertion of a central venous catheter into the cardiovascular system. Anesthesiology 1996;84:241–2. 140. Smyth NPD, Rogers JB. Transvenous removal of catheter emboli from the heart and great veins by endoscopic forceps. Ann Thorac Surg 1971;11:403–8. 141. Bossert T, Gummert J, Bittner H, et al. Swan-Ganz catheter-induced severe complications in cardiac surgery: right ventricular perforation, knotting, and rupture of a pulmonary artery. J Card Surg 2006;21:292–5. 142. Friedman BA, Jergeleit HC. Perforation of atrium by polyethylene central venous catheter. JAMA 1968;203: 1141–2. 143. Oropello J, Leibowitz A, Manasia A, et al. Dilator-associated complications of central venous catheter insertion: Possible mechanisms of injury and suggestions. J Cardiothorac Vasc Anesth 1996;10:634–7. 144. Royster RL, Johnston WE, Gravlee GP, et al. Arrhythmias during venous cannulation prior to pulmonary artery catheter insertion. Anesth Analg 1985;64:1214–6. 145. Eissa NT, Kvetan V. Guide wire as a cause of complete heart block in patients with preexisting left bundle-branch block. Anesthesiology 1990;73:772–4. 146. O’Grady NP, Alexander M, Dellinger EP, et al. Guidelines for the prevention of intravascular catheter-related infections. Infect Control Hosp Epidemiol 2002;23:759–69. 147. Hu KK, Lipsky BA, Veenstra DL, Saint S. Using maximal sterile barriers to prevent central venous catheter-related infection: a systematic evidence-based review. Am J Infect Control 2004;32:142–6. 148. Timsit JF, Sebille V, Farkas JC, et al. Effect of subcutaneous tunneling on internal jugular catheter-related sepsis in critically ill patients: a prospective randomized multicenter study. JAMA 1996;276:1416–20. 149. Timsit JF, Bruneel F, Cheval C, et al. Use of tunneled femoral catheters to prevent catheter-related infection. A randomized, controlled trial. Ann Intern Med 1999;130:729–35. 150. Leon C, Alvarez-Lerma F, Ruiz-Santana S, et al. Antiseptic chamber-containing hub reduces central venous catheter-related infection: a prospective, randomized study. Crit Care Med 2003;31:1318–24. 151. Veenstra DL, Saint S, Saha S, et al. Efficacy of antiseptic-impregnated central venous catheters in preventing catheter-related bloodstream infection: a meta-analysis. JAMA 1999;281:261–7. 152. Kamal GD, Pfaller MA, Rempe LE, Jebson PJR. Reduced intravascular catheter infection by antibiotic bonding: a prospective, randomized, controlled trial. JAMA 1991;265:2364–8. 153. Cicalini S, Palmieri F, Petrosillo N. Clinical review: new technologies for prevention of intravascular catheter-related infections. Crit Care 2004;8:157–62.

Chapter 7 – Central Venous and Pulmonary Artery Catheterization

154. Maki DG, Ringer M, Alvarado CJ. Prospective randomised trial of povidone-iodine, alcohol, and chlorhexidine for prevention of infection associated with central venous and arterial catheters. Lancet 1991;338:339–43. 155. Mimoz O, Pieroni L, Lawrence C, et al. Prospective, randomized trial of two antiseptic solutions for prevention of central venous or arterial catheter colonization and infection in intensive care unit patients. Crit Care Med 1996;24:1818–23. 156. Chaiyakunapruk N, Veenstra DL, Lipsky BA, Saint S. Chlorhexidine compared with povidone-iodine solution for vascular catheter-site care: a meta-analysis. Ann Intern Med 2002;136:792–801. 157. Mermel LA. Prevention of intravascular catheter-related infections. Ann Intern Med 2000;132:391–402. 158. Polderman KH, Girbes AR. Central venous catheter use. Part 2: infectious complications. Intensive Care Med 2002;28:18–28. 159. Poses RM, McClish DK, Smith WR, et al. Physicians’ judgments of the risks of cardiac procedures. Differences between cardiologists and other internists. Med Care 1997;35:603–17. 160. Shah KB, Rao TLK, Laughlin S, El-Etr AA. A review of pulmonary artery catheterization in 6245 patients. Anesthesiology 1984;61:271–5. 161. Lopez-Sendon J, Lopez de Sa E, Gonzalez Maqueda I, et al. Right ventricular infarction as a risk factor for ventricular fibrillation during pulmonary artery catheterization using Swan-Ganz catheters. Am Heart J 1990;119:207–9. 162. Spring CL, Pozen RG, Rozanski JJ, et al. Advanced ventricular arrhythmias during bedside pulmonary artery catheterization. Am J Med 1982;72:203–8. 163. Patil AR. Risk of right bundle-branch block and complete heart block during pulmonary artery catheterization. Crit Care Med 1990;18:122–3. 164. Abernathy WS. Complete heart block caused by a Swan-Ganz catheter. Chest 1974;65:349. 165. Thomson IR, Dalton BC, Lappas DG, et al. Right bundle-branch block and complete heart block caused by the Swan-Ganz catheter. Anesthesiology 1979;51:359–62. 166. Sprung CL, Elser B, Schein RMH, et al. Risk of right bundle-branch block and complete heart block during pulmonary artery catheterization. Crit Care Med 1989; 17:1–3. 167. Morris D, Mulvihill D, Lew WYW. Risk of developing complete heart block during bedside pulmonary artery catheterization in patients with left bundle-branch block. Arch Intern Med 1987;147:2005–10. 168. Hannan AT, Brown M, Bigman O. Pulmonary artery catheter-induced hemorrhage. Chest 1984;85:128–31. 169. Durbin CG. The range of pulmonary artery catheter balloon inflation pressures. J Cardiothorac Anesth 1990;4:39–42. 170. Dhamee MS, Pattison CZ. Pulmonary artery rupture during cardiopulmonary bypass. J Cardiothorac Anesth 1987;1:51–56. 171. Cohen JA, Blackshear RH, Gravenstein N, Woeste J. Increased pulmonary artery perforating potential of pulmonary artery catheters during hypothermia. J Cardiothorac Vasc Anesth 1991;5:234–6. 172. Stein JM, Lisbon A. Pulmonary hemorrhage from pulmonary artery catheterization treated with endobronchial intubation. Anesthesiology 1981;55:698–9. 173. Sirivella S, Gielchinsky I, Parsonnet V. Management of catheter-induced pulmonary artery perforation: a rare complication in cardiovascular operations. Ann Thorac Surg 2001;72:2056–9.

174. Purut CM, Scott SM, Parham JV, Smith PK. Intraoperative management of severe endobronchial hemorrhage. Ann Thorac Surg 1991;51:304–7. 175. Laureys M, Golzarian J, Antoine M, Desmet JM. Coil embolization treatment for perioperative pulmonary artery rupture related to Swan-Ganz catheter placement. Cardiovasc Intervent Radiol 2004;27:407–9. 176. Abreu AR, Campos MA, Krieger BP. Pulmonary artery rupture induced by a pulmonary artery catheter: a case report and review of the literature. J Intensive Care Med 2004;19:291–6. 177. Foote GA, Schabel SI, Hodges M. Pulmonary complications of the flow-directed balloon-tipped catheter. N Engl J Med 1974;290:927–31. 178. Ahmed H, Kaufman D, Zenilman M. A knot in the heart. Am Surg 2008;74:235–6. 179. Mond HG, Clark DW, Nesbitt SJ, Schlant RC. A technique for unknotting an intracardiac flow-directed balloon catheter. Chest 1975;67:731–733. 180. England MR, Murphy MC. A knotty problem. J Cardiothorac Vasc Anesth 1997;11:682–3. 181. Eshkevari L, Baker B. Occurrence and removal of a knotted pulmonary artery catheter: a case report. AANA Journal 2007;75:423–8. 182. Georghiou GP, Vidne BA, Raanani E. Knotting of a pulmonary artery catheter in the superior vena cava: surgical removal and a word of caution. Heart 2004;90:e28. 183. Arnaout S, Diab K, Al-Kutoubi A, Jamaleddine G. Rupture of the chordae of the tricuspid valve after knotting of the pulmonary artery catheter. Chest 2001;120:1742–4. 184. Bagul N, Menon N, Pathak R, et al. Knot in the cava – an unusual complication of Swan-Ganz catheters. Eur J Vasc Endoovasc Surg 2005;29:651–3. 185. Lazzam C, Sanborn TA, Christian F. Ventricular entrapment of a Swan-Ganz catheter: A technique for nonsurgical removal. J Am Coll Cardiol 1989;13:1422–4. 186. Sherman S, Wall M, Kennedy D et al. Do pulmonary artery catheters cause or increase tricuspid or pulmonic valvular regurgitation? Anesth Analg 2001:92:1117–22. 187. Boscoe MJ, deLange S. Damage to the tricuspid valve with a Swan-Ganz catheter. BMJ 1981;283:346–7. 188. O’Toole JD, Wurtzbacher JJ, Wearner NE, Jain AC. Pulmonary valve injury and insufficiency during pulmonary-artery catheterization. N Engl J Med 1979;301:1167–8. 189. Kainuma M, Yamada M, Miyake T. Pulmonary artery catheter passing between the chordae tendineae of the tricuspid valve [correspondence]. Anesthesiology 1995;83:1130. 190. Rowley KM, Clubb KS, Smith GJ, Cabin HS.: Right-sided infective endocarditis as a consequence of flow-directed pulmonary-artery catheterization. A clinicopathological study of 55 autopsied patients. N Engl J Med 1984;311:1152–6. 191. Greene JF Jr, Fitzwater JE, Clemmer TP. Septic endocarditis and indwelling pulmonary artery catheters. JAMA 1975;233: 891–2. 192. Kim YL, Richman KA, Marshall BE. Thrombocytopenia associated with Swan-Ganz catheterization in patients. Anesthesiology 1980;53:261–2. 193. Hofbauer R, Moser D, Kaye AD, et al. Thrombus formation on the balloon of heparin-bonded pulmonary artery catheters: an ultrastructural scanning electron microscope study. Crit Care Med 2000;28:727–35. 194. Mangano DT. Heparin bonding and long-term protection against thrombogenesis. N Engl J Med 1982;307:894–5.

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195. Moberg PQ, Geary VM, Sheikh FM. Heparin-induced thrombocytopenia: A possible complication of heparin-coated pulmonary artery catheters. J Cardiothorac Anesth 1990;4:226–8. 196. Tewari P, Kumar M, Kaushik S. Pulmonary artery catheter misplaced in liver. J Cardiothorac Vasc Anesth 1995;9:482–4. 197. Karakaya D, Baris S, Tur A. Pulmonary artery catheter-induced right ventricular perforation during coronary artery bypass surgery. Br J Anaesth 1999;82:953. 198. Shin B, McAslan TC, Ayella RJ. Problems with measurements using the Swan-Ganz catheter. Anesthesiology 1975;43:474–6. 199. American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Practice guidelines for pulmonary artery catheterization: an updated report by the American Society of Anesthesiologists Task Force on Pulmonary Artery Catheterization. Anesthesiology 2003;99:988–1014. 200. Robin ED. Defenders of the pulmonary artery catheter. Chest 1988;93:1059–66. 201. Dalen JE, Bone RC. Is it time to pull the pulmonary artery catheter? JAMA 1996;276:916–8. 202. Zaidan J, Freniere S. Use of a pacing pulmonary artery catheter during cardiac surgery. Ann Thorac Surg 1983;35:633–6. 203. Mora CT, Seltzer JL, McNulty SE. Evaluation of a new design pulmonary artery catheter for intraoperative ventricular pacing. J Cardiothorac Anesth 1988;2:303–8. 204. Trankina MF, White RD. Perioperative cardiac pacing using an atrioventricular pacing pulmonary artery catheter. J Cardiothorac Anesth 1989;3:154–62.

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205. Risk SC, Brandon D, D’Ambra MN, et al. Indications for the use of pacing pulmonary artery catheters in cardiac surgery. J Cardiothorac Vasc Anesth 1992;6:275–80. 206. Kay HR, Afshari M, Barash P, et al. Measurement of ejection fraction by thermal dilution techniques. J Surg Res 1983;34:337–46. 207. Spinale FG, Zellner JL, Mukherjee R, Crawford FA. Placement considerations for measuring thermodilution right ventricular ejection fraction. Crit Care Med 1991;19:417–21. 208. Assmann R, Heidelmeyer CF, Trampisch HJ, et al. Right ventricular function assessed by thermodilution technique during apnea and mechanical ventilation. Crit Care Med 1991;19:810–7. 209. Krouskop RW, Cabatu EE, Chelliah BP, et al. Accuracy and clinical utility of an oxygen saturation catheter. Crit Care Med 1983;11:744–9. 210. Reinhart K, Kuhn HJ, Hartog C, Bredle DL. Continuous central venous and pulmonary artery oxygen saturation monitoring in the critically ill. Intensive Care Med 2004;30:1572–8. 211. Scuderi P, MacGregor D, Bowton D, et al. A laboratory comparison of three pulmonary artery oximetry catheters. Anesthesiology 1994;81(1):245–53. 212. Pond CG, Blessios G, Bowlin J, et al. Perioperative evaluation of a new mixed venous oxygen saturation catheter in cardiac surgical patients. J Cardiothorac Vasc 1992;6:280–2. 213. Armaganidis A, Dhainaut JF, Billard JL, et al. Accuracy assessment for three fiberoptic pulmonary artery catheters for SvO2 monitoring. Intensive Care Med 1994;20:484–8.

Chapter

8

Cardiac output and intravascular volume Mukul Kapoor and Marc Stone

It is absolutely necessary to conclude that the blood in the animal body is impelled in a circle, and is in a state of ceaseless motion; that this is the act or function which the heart performs by means of its pulse; and that it is the sole and only end of the motion and contraction of the heart. William Harvey (1578–1657)

Introduction The management of a hemodynamically unstable patient is one of the most challenging experiences for the acute care physician; incorrect treatment or delay in appropriate treatment can result in morbidity and mortality. Anesthesia- and sepsis-induced changes in arterial or venous tone, intravascular volume, ventricular performance, peripheral vascular reactivity, core temperature, and blood rheology sum to make the moment-tomoment assessment of cardiovascular status difficult. Monitoring the heart rate and blood pressure may be adequate for many patients, but in a milieu of cardiovascular abnormality, more detailed measurements are needed, as the cardiovascular system is too complex for assessment with something as ingenuous as heart rate and systemic blood pressure.1 Hypovolemia, systemic vasodilation, and myocardial dysfunction are frequently responsible for hemodynamic instability during the perioperative period and in the intensive care unit. An accurate assessment of cardiac preload is of paramount importance in critically ill patients with true/relative hypovolemia to direct therapy and optimize the cardiac output. Although the majority of patients with hemodynamic compromise are preload-responsive, excessive fluid administration will provoke fluid overload in the remaining ones.2 Cardiac filling pressures, measured using a pulmonary artery catheter (PAC), are still widely used to guide fluid therapy in major surgery and critical care, but critical analysis of clinical studies has shown that cardiac filling pressures are of little value to predict ventricular filling volume, or the hemodynamic effects of intravascular volume expansion.3,4 The first method to measure cardiac output (CO) in humans was described by Adolf Fick in 1870.5 In 1954, Fegler introduced CO measurement by thermodilution, but it was the development of the balloon-tipped PAC by Swan and Ganz in the 1970s that made the technique more practicable.6 The PAC was initially used to measure intracardiac pressures, but CO

measurement later became its primary function. At the time of this writing, the PAC remains the gold-standard device for determination of CO, although it is hardly ideal, for a variety of reasons (discussed subsequently). An ideal device to measure CO would be continuous, automated, self-calibrating, easy to use, and noninvasive. It would rapidly provide an accurate and comprehensive measure of cardiac performance (contractility, preload, and afterload) in an operator-independent, cost-effective, and reproducible manner, without increasing morbidity and mortality.7,8 A number of devices to estimate CO have since been introduced, but the search for an ideal CO monitor continues. This chapter discusses the basic and essential principles underlying determination of CO by various methodologies. Specific devices that employ the different methodologies are discussed, including PAC, NICO, CCCombo, OptiQ CCO/Qvue, truCATH, PiCCO, LiDCO, Finometer, FloTrac/Vigileo, endotracheal CAO monitor (ECOM), and ultrasonic CO monitor (USCOM). The chapter concludes with discussions of complications, accreditation, and practice parameters.

Technical aspects of the measurement of cardiac output Systems based on Fick’s principle Fick’s principle is based on the conservation of mass. Fick postulated that all oxygen taken up by the lungs is completely transferred to the blood, and the oxygen consumption per unit time is the product of blood flow through the lungs and the arteriovenous oxygen content difference. The application of the principle provides an accurate and reproducible measure of CO. The arterial–mixed venous oxygen content difference is calculated by analysis of arterial and mixed venous blood samples, drawn from an arterial line and the distal port of a PAC, respectively, whereas the oxygen consumption is calculated by inspired/expired gas analysis and minute ventilation. CO is calculated by relating oxygen consumption to arterial and mixed venous oxygen content using the equation Q = [VO2 /(CaCo2 − CvCO2 )] × 100, where Q is the cardiac output, VO2 is the oxygen consumption (content difference between inspired and exhaled gas), CaO2 is

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oxygen content of arterial blood, and CvO2 is oxygen content of mixed venous blood. This estimation is accurate when the hemodynamic status is sufficiently stable to allow constant gas diffusion during transit of blood through the lungs. However, the estimation may not be valid in critically ill patients with unstable hemodynamics and who require high fractional inspired oxygen. In theory, Fick’s technique is the gold standard for cardiac output measurement, but it is invasive, complex in methodology, and difficult to perform.

Differential carbon dioxide Fick partial rebreathing technique A modification of the Fick principle is used in the differential carbon dioxide partial rebreathing method used by the NOVA NICO monitor (Novametrix Medical Systems; Wallingford, CT). Changes in CO2 elimination and partial pressure of end-tidal CO2 following a brief period of partial rebreathing are used to estimate pulmonary capillary blood flow, instead of oxygen consumption, as CO2 elimination is easier to measure. The rebreathing maneuver is used to estimate mixed venous partial pressure of CO2 , which, combined with concurrent measurements of end-tidal CO2 and CO2 production, gives a noninvasive estimate of CO.9 The monitor offers the advantage of also measuring CO2 production, continuous tidal volumes and flows, and compliance assessment on a breath-by-breath basis, and provides a continuous estimate of metabolic demand. The NOVA NICO rebreathing circuit can be incorporated into both the anesthesia machine breathing circuit and the ventilator circuit (Figure 8.1). Rebreathing CO2 reduces the blood–alveolar gradient and thereby reduces the CO2 flux. This elevates arterial CO2 content, which restabilizes during the next baseline phase. CO2 data

Automatic rebreathing valve ‘Y’ piece

Carbon dioxide sensor Carbon dioxide flow sensor

Breathing Circuit

NICO Loop (adjustable rebreathing volume)

Figure 8.1. NOVA NICO breathing circuit. A pneumatically controlled rebreathing valve is sited within a large- bore tubing loop and a CO2 /flow sensor in the ventilator circuit between the patient and the Y-connector. The rebreathing valve cycles through two phases. During the first phase, the rebreathing valve directs the flow straight through the valve, whereas during the second phase, positive pressure activates the valve to direct the endexpired gas into the expandable large-bore tubing loop. This end-exhaled gas is accumulated for inspiration during the patient’s next breath. (Modified from ref. 8, permission granted).

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measured during the rebreathing and the nonrebreathing periods is used to calculate the ratio of the change in CO2 elimination and computation of CO10 using the formula Q = VCO2 /(CvCO2 − CaCO2 ), where Q is the cardiac output, VCO2 is the carbon dioxide output (content difference between exhaled and inspired gas), CaCO2 is the carbon dioxide content of arterial blood, and CvO2 is the carbon dioxide content of mixed venous blood. Clinical trials with NICO have shown reasonably good correlation with CO measured by thermodilution CO (TDCO).11,12 However, the monitor requires stable CO2 elimination for reliable CO measurements and has been reported to be unreliable at low-volume minute ventilation and in spontaneous breathing;13 during rapid changes in pulmonary shunts and dead-space, as in thoracic surgery;14 and after cardiopulmonary bypass and aortic clamping/unclamping.15 In intensive care, as the majority of patients are ventilated with modes that allow some spontaneous breathing, the use of the device is limited to patients who are deeply sedated or anesthetized and/or paralyzed.16 Although the technology was introduced nearly two decades ago, its use remains limited.

Systems based on indicator dilution The principle of indicator dilution for measuring CO was first described by Stewart.17 These methods make use of the time taken by flowing blood to dilute an indicator substance introduced to the circulatory system at a given point until it reaches a point downstream to obtain a time dilution curve. Usually these methods require a PAC because the indicator substance must be introduced at a point at which uniform mixing will occur within the total blood flow, prior to the measurement of a dilution curve. The average volume flow is inversely proportional to the integrated area under the dilution curve. The CO, being inversely proportional to the concentration of the indicator sampled downstream, is estimated using the Stewart– Hamilton principle, wherein CO is estimated from the quantity of indicator injected divided by the area under the dilution curve measured downstream.

Dye dilution A known quantity of dye (normally indocyanine green) is injected into the pulmonary artery, and timed arterial samples are analyzed using a photoelectric spectrometer. Plotting the concentration of dye against time on a semilogarithmic plot (with extrapolation of the straight line created to correct for dye recirculation) allows calculation of cardiac output by the mass of injectate used and the area under the extrapolated curve.

Lithium indicator dilution A bolus of isotonic lithium chloride solution is injected via a central or peripheral vein. The lithium concentration–time curve is recorded by withdrawing arterial blood past a lithium sensor attached to the arterial line. CO is calculated from the

Chapter 8 – Cardiac Output and Intravascular Volume

lithium dose and the area under the concentration–time curve prior to recirculation. Blood flows into the sensor assembly at a rate controlled by a peristaltic pump. A bolus dose of 0.15 to 0.30 mmol of lithium chloride is needed for an average adult.

Thermodilution cardiac output

Temperature change in Pulmonary Artery °C

Pulmonary artery thermodilution methods use change of temperature of blood flowing in the right-sided circulation for the measurement of blood flow. The thermodilution principle is based on the injection of a quantified cold charge and registration of its dilution (i.e. the subsequent change in temperature of the blood at a point downstream in the direction of the blood flow). As heat, unlike a dye, will mix well irrespective of laminar flow in the blood vessels, the thermoindicator can be injected into the right atrium and the temperature registered in the pulmonary artery. The TDCO method uses a cold solution to create a thermal deficit as a variant of the indicator–dilution method. A known bolus of a cold sterile solution is injected, as a thermal indicator, into the right atrium through the proximal port of a PAC. A thermistor located at the distal end of the PAC detects the change in temperature of the blood downstream. The distance between the injection and detection sites should be as short as possible to reduce extravascular loss of the thermal indicator owing to heat exchange in the pulmonary vascular bed. This can be attained by injecting into the right atrium and detection in the PA. The normal thermodilution curve peaks rapidly and then follows an exponential decay, until there is recirculation or delayed cooling from the residual indicator in the PA catheter (Figure 8.2). CO is inversely proportional to the area under the curve (temperature change over time). A small area under the curve indicates a high CO. The faster blood flows through the heart, the earlier the peak and sharper the drop, because the catheter senses temperature change over a short period.

1.0

Cold injectate at thermistor

0.8

End of curve plotted

0.6 0.4

Peak Temperature

Baseline temperature fluctuations coinciding with phase of respiration

Injectate

0.2 0 Time

Figure 8.2. Typical thermodilution curve. CO is determined using the  Stewart–Hamilton equation: Q = K1 × K2 × VI × (TB -TI )/ Tb (t) dt, where Q is the cardiac output; K1 is a density factor defined as the specific heat multiplied by the specific gravity of the injectate divided by the product of the specific heat and gravity of blood; K2 is a computation constant taking into account the catheter dead space, the heat exchange in transit, and injection rate; VI is the volume of injectate; TB and TI the initial temperature of the blood and injectate respectively; and Tb(t) dt is the change of blood temperature as a function of time and corresponds to the area under the thermodilution curve.

A low cardiac output results in a larger area under the curve. When blood flows slowly (low cardiac output), the area under the curve is greater because the catheter senses changes in temperature over a longer period. The change in temperature of blood in the PA causes a change in the thermistor (Wheatstone bridge) resistance, which allows calculation of the area under the thermodilution curve. A correction factor is introduced for the loss of indicator by transit of the cold solution through the catheter into the right atrium. From the Stewart–Hamilton equation, the cardiac output is calculated by a computer, and a thermodilution curve also can be recorded. As there are limits to the numerical values the computer can handle, the computation factor must be altered for very low and for very high outputs. Even under ideal circumstances, TDCO measurements have a 10 percent error rate.18,19 The accuracy of the thermodilution technique can be influenced by various factors: 1. Presence of a cardiac shunt: right and left ventricular output may differ. 2. Tricuspid or pulmonary valve regurgitation: backflow of blood and indicator causes underestimation of CO. 3. Variations in blood temperature affecting measurements: after cardiopulmonary bypass, intravenous fluid administration. 4. Speed of the bolus injection and its timing relative to the phase of the respiratory cycle: positive pressure ventilation produces beat-to-beat variations in right ventricular stroke volume during the cycle. 5. Positive end-expiratory pressure. 6. Catheter dysfunction and position of the PAC. 7. Volume and temperature of the injectate. 8. Patient’s body position. To ensure the validity and reliability of the measurement, the following should be checked meticulously: r Position of the pulmonary artery catheter r Computation constant of the pulmonary artery catheter (PAC) r Catheter size r Temperature of the injectate r Volume of injectate, 10 mL at room temperature (5 mL if iced) The difference between the temperature of the injectate and the temperature of the patient’s blood should be 10◦ C.20 Ten mL of iced injectate produces a greater signal-to-noise ratio than does ten mL of room-temperature injectate or smaller volumes of either iced. Pearl and colleagues recommended the use of 10 mL iced or room-temperature injectate for CO determinations, because 10-mL injectates produced less variability than 3 or 5 mL of injectate.21 Most reports show no difference in the accuracy or reproducibility whether iced or room-temperature injectate was used.21,22 To accurately measure CO, inject cold saline at a constant rate (10 mL within 4 seconds; 5 mL within 2 seconds) during

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end expiration, using a closed injectate delivery system. Obtain three measurements and assess the cardiac output curve. The average value computed should be within 10 percent of the median value.

Continuous CO monitoring Advances in technology have allowed for the development of continuous CO monitoring by the use of a random sequence of temperature changes generated by a heating coil within the PAC, which is located in the right ventricle (CCOmbo/Vigilance, Edwards Lifesciences LLC, Irvine, CA; Opti Q CCO/Q-vue, Abbott Critical Care Systems, Mountain View, CA). A monitor computes the CO in real time from the fractional changes in temperature detected distally. The heat impulses are generated in a stochastic pattern, and subsequent processing allows for automated updating of CO within minutes.23 The heating filament is cycled on and off in a pseudorandom sequence, and CO is calculated using a cross-correlation algorithm that combines the measured pulmonary artery temperature and the pseudorandom sequence of filament activation.24 A faulty thermal filament, blood temperature ≤31◦ C or ≥41◦ C, electrical interference from electrocautery, and large blood temperature variations can affect calculations. Other specialized pulmonary artery catheters are available that also use the principle of mass heat transfer. The truCATH (BD Medical Systems) obtains data from the measured amount of energy required to maintain a thermistor, located in the right atrium, at 1◦ C above the measured blood temperature in the pulmonary artery. Delays in data acquisition prevent these systems from being truly real-time, as there is an inherent delay in response to sudden flow changes. However, there is a reduced need for bolus injections and they provide a better average CO over time compared with intermittent bolus techniques. These systems offer the advantages of possibly being more accurate, convenient, and user-independent; reducing demands on the time of carers; and providing an early signal of hemodynamic alterations.23,25 The passage of the PAC catheter into the right-sided circulation has the added advantage of measuring the right atrial, pulmonary artery, and the pulmonary artery occlusion pressure.

Pressure (mmHg)

Estimation of the preload of the cardiac chambers – and, indirectly, the intravascular volume – is thus possible. Advances in computation techniques have also resulted in development of algorithms to calculate the global end-diastolic volume and the right ventricular end-diastolic and end-systolic volumes, facilitating better estimation of the intravascular blood volume.26 With advances in technology, the continuous CO catheters have also been incorporated with oximetry sensors to continuously measure mixed venous oxygen saturation online.

Systems based on pulse contour analysis Arterial pulse contour analysis was first described in the early 1940s. It is a technique to measure and monitor stroke volume on a beat-to-beat basis from the arterial pulse pressure waveform and is based on the principle that the magnitude of the arterial pulse pressure and the pressure decay profile describe a unique stroke volume for given arterial input impedance (Figure 8.3). A number of devices are commercially available that provide CO data following calibration by an independent CO measurement. Some of them require central venous access to perform a TDCO measurement for calibration (analyzed by a thermistor present in the arterial catheter tip), but cannulation of the right heart or pulmonary artery is not required. Based on models representing the systemic circulation, several methods are used to analyze the pressure waveform, which include the Windkessel model, its modification, and new advanced models. The basic Windkessel model (twoelement model – aortic impedance, arterial and peripheral vascular resistance) assumes that the time constant of the monoexponential pressure decay is determined by the product of systemic vascular resistance and aortic compliance, whereas the modified Windkessel model (three-element model- aortic impedance, arterial compliance, and peripheral vascular resistance), assumes that compliance of the arterial system can be partitioned into central and distal compartments, in which central compliance is distinct from distal compliance.27,28 Mechanical ventilation induces cyclic variations in cardiac preload that are reflected in changes in aortic blood flow and arterial pulse pressure within a period of a few pulses.29

120 Area under systolic curve

Area under diastolic curve

80

Systole

Diastole

Time

Figure 8.3. Pulse contour analysis waveform. The area under the measured waveform is analyzed to derive ejection systolic area by identifying ventricular ejection and the appearance of the dicrotic notch (closure of the aortic valve). The pulsatile systolic area under the pressure curve above a horizontal line drawn from the diastolic point and bounded by a vertical line through the lowest point of incisura (area under the pressure curve from the start of the upstroke to the incisura) and stroke volume are related by means of characteristic impedance of the aorta.

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Chapter 8 – Cardiac Output and Intravascular Volume

Maximum systolic pressure

120 110

Minimum systolic pressure

100 Arterial 90 pressure 80 (mmHg) 70

Maximum stroke volume Minimum stroke volume

25

Paw

Time

20 15 Airway 10 pressure 5 (cm H2O)

Inspiration

Expiration

Time

Figure 8.4. Pulse pressure and stroke volume variations, as functional hemodynamic variables, are based on the heart–lung interactions during mechanical ventilation. Respiration-induced changes in left ventricular preload result in cyclic changes in left ventricular stroke volume and in arterial pressure. The left ventricular stroke volume increases during inspiration because left ventricular preload increases, whereas left ventricular afterload decreases. In hypovolemic patients, the respiratory variations in stroke volume and arterial pressure are of greater magnitude because the venous system is more collapsible. The pulse contour analysis, based on the computation of the area under the systolic portion of the arterial pressure curve, allows a beat-to-beat measurement of left ventricular stroke volume and the quantification of its variation during a short period of a few seconds.

The arterial pulse pressure variation and stroke volume variation, induced by mechanical ventilation, have been shown to be useful in identifying patients likely to respond to volume therapy.2,30–32 Arterial pulse contour analysis allows the use of arterial pressure waveforms to calculate stroke volume and its change during ventilation, and thus helps determine pulse pressure variation and stroke volume variation (Figure 8.4). The technique helps calculates CO changes and assess global cardiovascular responsiveness to therapies such as fluid and inotropes. The ratio of pulse pressure variation to stroke volume variation reflects the central capacitor tone, whereas the ratio of mean arterial blood pressure changes to stroke volume variation reflects the arterial tone. The technique thus helps monitor both the arterial and venous tone, which are major determinants of cardiovascular performance. Concerns have been raised about issues that affect the accuracy of pulse contour analysis-based systems.33 The major issues raised are

arterial catheter. The stroke volume is estimated from the systolic, diastolic, or both components of the pressure waveform. However, these algorithm-based estimations fail to remain accurate in aortic regurgitation, with use of high-dose vasodilators or vasoconstrictors, and with the use of intraaortic balloon pumps.34

r Nonlinearity of the waveform will affect the algorithm-based calculations, as the compliance of the aorta varies at different arterial pressures. Properties of the aorta also vary with age, gender, distending pressure, and atherosclerosis. Aortic valve pathology, aortic aneurysms, and sympathetic outflow status also influence aortic characteristics. r The aortic pulse waveform reflects the stroke volume. However, the peripheral arterial pressure waveform (which has higher resonance) is used for monitoring, and thus there is a need for accurate compensation with antiresonance. In addition, continuous flush devices need to be used because damped waveforms may result in an inaccurate assessment of CO. r Supine/prone position and increased abdominal pressure in obesity may affect aortic distending properties.

Systolic pulse contour analysis

The available devices use varied patented algorithms but essentially provide a continuous estimate of CO through analysis of the shape of the pulse wave from a peripherally placed

Diastolic pulse contour analysis Diastolic pulse contour analysis is based on the basic Windkessel model and assumes that the arterial blood pressure should decay exponentially during diastolic time intervals with a time constant. By fitting the diastolic decay portion of an individual’s arterial waveform to a first-order model (basic Windkessel) or third-order model (modified Windkessel), compliance variables can theoretically be derived. In this model, because the arterial compliance is assumed to be constant, the derived stroke volume values do not reflect the true stroke volume. For accurate values, calibration against a standard method is carried out.

Wesseling and coworkers developed a pulse contour analysis technique based on a transmission line model of the arterial tree. The Wesseling algorithm involves measuring the systolic portion of the ejection phase divided by aortic impedance to provide a measure of stroke volume.35 The algorithm uses the three major properties of the aorta and the arterial system (aortic impedance, Windkessel compliance of the arterial system, and peripheral vascular resistance) to compute a flow pulse from an arterial pressure pulsation.36 According to the Wesseling model, total systemic vascular resistance is a time-varying property of the vascular bed.37 CO determined by an independent alternative method is used to calibrate the device. The PiCCO system (Pulsion Medical System; Munich, Germany) is a commercially available continuous CO monitor with a working principle based on the preceding model. However, it differs from this model in that no age-related corrections for pressure-dependent nonlinear changes in aortic cross-sectional area are incorporated. In the newer version of the equipment, the algorithm analyzes the actual shape of the

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Monitoring in Anesthesia and Perioperative Care

waveform, in addition to computing the pulsatile systolic area.38 With improvement in computation technology, the device can measure vascular volumes from advanced analysis of the thermodilution curve. In the PiCCO system, a 20-cm–long arterial catheter with a thermistor embedded in its wall is inserted in the femoral artery. The arterial catheter is connected to the pulse contour analysis computer for monitoring of arterial blood pressure, heart rate, temperature, and measurements derived from the arterial pressure wave. The device is initially calibrated by TDCO measurements, randomized within the respiratory cycle, by injection of saline solution at a temperature lower than 7◦ C via a central venous catheter, and the subsequent detection of the cold saline injection by the thermistor in the arterial catheter. Beat-to-beat calculations are averaged over 30-second cycles and displayed as a numerical value. Continuous CO assessed by PICCO and by TDCO have been found to be comparable by a number of studies; however, the monitor needs to be recalibrated if the systemic vascular resistance changes markedly.37,39–41

Modelflow pulse contour analysis The Modelflow method computes an aortic flow waveform from the arterial pressure waveform using the three-element model developed by Wesseling and associates.36 It computes the arterial flow waveform from the pressure waveform with continuous nonlinear corrections for variations in aortic diameter, impedance, and compliance during the arterial pulsation. The patient’s gender, age, height, and weight are entered into the Modelflow computer to determine pressure–volume, pressure– compliance, and pressure–characteristic impedance relationships using Langewouters’ equations, which are based on population averages. This model is simulated digitally in real time and supplied with the sampled arterial pressure waveform.42 The aortic impedance is a function of aortic cross-sectional area, the instantaneous flow, and compliance. Postmortem studies have shown that aortic cross-sectional area is a function of pressure by an arctangent relation and also of the patient’s age, gender, height, and weight.43,44 The aortic impedance and arterial compliance are computed making use of a built-in database of arctangent area–pressure relationships derived from these studies. Both compliance and impedance are nonlinear and are functions of the elasticity of the aorta. This nonlinear property is taken into account to calculate stroke volume and is presented in terms of the aortic pressure area relation and its derivative. The subject’s gender and age are also input. The instantaneous impedance and compliance values obtained are used in a model simulation to compute an aortic flow waveform. The peripheral vascular resistance is calculated for each beat and updated. Integration of flow waveform per beat gives stroke volume. The Finometer (Finapres Medical Systems BV; Amsterdam, The Netherlands) is a noninvasive blood pressure measurement monitor that uses proprietary Modelflow methodology to provide beat-to-beat CO monitoring. The system can operate noninvasively by using the volume–clamp method of obtaining

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finger arterial pressure tracings with the Physiocal algorithm to periodically correct the system for changes such as hematocrit, physiologic stress, or smooth muscle tone. The system includes a servo-controlled pressure device for applying the rapidly changing pressures to the finger-pressure cuff as well as a photoplethysmography light source and a detector for application of the volume–clamp method. The front-end unit is connected to the Finometer for finger arterial tracing determination, brachial pressure derivations, and CO determinations. The system has the ability to trend changes in CO. However, if absolute CO values are desired, a calibration with another CO determination is necessary.38 The Modelflow and Finometer have been reported as inaccurate when evaluated against TDCO.45,46 However, when the devices are calibrated by an independent mode of CO determination, the CO values are reliable and accurate.47,48

Pulse power analysis The arterial blood pressure waveform measured in a peripheral artery arises from the interaction between the arterial system and the heart (i.e. an incident pressure wave ejected from the heart and a reflected wave from the peripheral arterial system). At any point in the arterial system, a measured waveform may be decomposed into its forward and backward components. Theoretically, if wave reflection were absent, then the pressure and flow contours in the aorta would be identical, their magnitudes being related by the aortic characteristic impedance. Differences between the pressure and flow contours in the aorta occur because backward waves result in augmentation of the pressure but retardation of the flow. Depending on the distance of the sampling site from the heart and the patient’s age, the reflected wave characteristics change. To calculate stroke volume, the two waves need to be analyzed individually.49 The algorithm used is based on the assumption that the net power change in a cardiac cycle is stroke volume, less the blood lost to the periphery during the beat, and that the net power and net flow relate to each other. The algorithm used thus caters to this aspect. The method is independent of the position of the sampling site, as the whole beat is analyzed. The pressure wave is transformed to a volume wave and the net power and beat period are derived from the volume waveform, using autocorrelation. Net power is proportional to net flow. Changes in stroke volume, rather than absolute values, are calculated using this method. 49 Popular commercial equipment that make use of pulse power analysis include the LiDCO plus (LiDCO Ltd; Cambridge, UK) and the Flo Trac/Vigileo (Edwards Lifesciences LLC; Irvine, CA). Both the devices use proprietary algorithms to derive CO and other derived parameters. Similar to the PiCCO system, both these devices also display the pulse pressure variation and the stroke volume variation, which are indicative of the patient’s intravascular volume status. The LiDCO system needs to be calibrated using the lithium dilution technique, by placing 0.3 mmol of lithium chloride in an indwelling central venous line and then flushing this

Chapter 8 – Cardiac Output and Intravascular Volume

line rapidly with 20 mL of 0.9% saline, ensuring a rapid bolus of lithium chloride entering into the circulation. A lithiumspecific sensor connected to the arterial line detects the change in lithium ion concentration in blood coming in contact with it and generating a lithium indicator dilution curve to derive the CO. Although this dose has no known pharmacological effect, the technique is contraindicated in patients receiving therapeutic lithium. High doses of neuromuscular blocking agents, with quaternary ammonium ions, can interfere with the sensing electrode; hence, lithium calibration should be performed prior to the administration of these agents.38 The Flo Trac/Vigileo system can derive CO from the arterial waveform without the need for an independent method of calibration. It bases its calculations on arterial waveform characteristics in conjunction with patient demographic data. CO can be measured directly from a conventional arterial line attached to the sensor of the monitor, making CO monitoring appear “deceptively simple.”34 The performance of LiDCO and the Flo Trac has been evaluated vis-`a-vis PAC and found to be comparable in patients.50 CO value measures were found to be interchangeable with TDCO in 80 percent of uncomplicated cardiac surgical patients.51 However, CO measurements by the devices have been reported as inaccurate in hyperdynamic circulations;52 in the presence of altered arterial pressure waveform, as in aortic regurgitation and aortic counter-pulsation;53 and in the presence of alterations of vascular tone.54

Pressure-recording analytical method The pressure-recording analytic method (PRAM) determines continuous CO changes from the arterial pressure wave via mathematic analysis of the arterial pressure profile changes. It is a technique based on the mathematical analysis of pulse profile changes based on the theory of perturbations, by which any physical system under the effect of a perturbation tends to react to achieve its own state of minimum energy. The basic principle is that in any given vessel, volume changes occur mainly because of radial expansion of the artery in response to variations in pressure. The method analyzes the arterial pressure wave from a standard peripheral or centrally inserted arterial catheter, without need for independent CO calibration. The algorithm does not use retrospectively collected aortic impedance and compliance data obtained. PRAM analyzes the entire waveform, including the systolic ejection, compliance, and impedance, as well as the diastolic portion of flow related to peripheral vascular resistance. The technique recognizes that volume changes in the arterial system are related primarily to the radial expansion of the system in response to blood pressure changes. Involved in this process are the force of cardiac ejection, aortic impedance to inflow into the aorta, arterial compliance that elastically stores energy of the cardiac ejection, and the vascular resistance providing retrograde reflections.38 In an animal study, the PRAM device was reported to measure CO comparable with TDCO, during various hemodynamic states.55

Systems based on electrical impedance cardiography William Kubicek and National Aeronautical and Space Administration (NASA) researchers developed thoracic electrical bioimpedance to study cardiovascular hemodynamics of astronauts in absence of gravity – that is, under conditions mimicking space.56 Kubicek described the thorax as a cylinder evenly perfused with blood of specific resistivity, but Sramek later showed that the thorax behaves electrically more like a truncated cone.57 Aortic blood volume varies during systole and diastole, which results in a phasic change in electrical resistance through the thorax during the cardiac cycle. The technique involves continuous measurement of this change in impedance, caused by a fluctuation of blood volume, to measure and calculate stroke volume, CO, myocardial contractility, and total thoracic fluid status. The electrodes define the upper and lower limits of the thorax, and the distance between them is measured to obtain the thoracic length (Figure 8.5). A high-frequency, low-amplitude alternating current is introduced through the transmitting thoracic electrodes; the sensing thoracic electrodes measure impedance associated with the blood flow in the aorta during the cardiac cycle. By measuring the impedance changes during the pulse flow and the time intervals between these changes, stroke volume can be calculated. Increased blood volume, flow velocity, and alignment of red blood cells reduce impedance during systole, whereas the opposite effects during diastole increase impedance (Figure 8.6). Stroke volume can be determined from the impedance curve by extrapolating to the impedance change that would result if no blood were to flow out of the thorax during systole. Impedance change is approximated by drawing a tangent to the impedance

Injecting electrode Sensing electrode RA ECG

LA ECG

Sensing electrode Injecting electrode LL ECG Figure 8.5. Thoracic bioimpedance. Four pairs of electrodes and a set of ECG leads are used to measure the impedance changes and, thereby, the hemodynamic parameters. Each pair of electrodes consists of a transmitting and a sensing electrode. Two pairs are applied to the base of the neck on directly opposite sides, and two pairs are placed at the level of the sterno–xiphoid junction, directly opposite from each other.

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Monitoring in Anesthesia and Perioperative Care

ECG

R T

P

S

Bioimpedance

dZ/dt max

dZ/dt

Stroke volume

Z0

Ventricular ejection time

Time

Figure 8.6. Bioimpedance. The change in impedance is measured from the baseline impedance (Z0 ), which reflects total thoracic fluid volume. The change in impedance related to time (dZ/dt) generates a waveform similar to the aortic flow curve and is a reflection of left ventricular contractility. Simultaneous ECG recording helps calculation of ventricular ejection time of each cardiac cycle.

curve at the point of its maximum rate of change. The stroke volume is calculated using the formula Stroke Volume = ␳ ×L 2 /Z02 x(d Z/dt)max ×VET where ␳ is the resistivity of blood, L is the mean distance between the inner electrodes, VET is the ventricular ejection time, (dZ/dt)max is the maximum value of change in impedance relative to time, and Z0 is the basal thoracic impedance. VET is obtained from the dZ/dt versus time curve and ECG. Electrocautery, mechanical ventilation, and surgical manipulations distort the impedance signal, leading to inaccurate readings. Alterations in cardiac performance resulting from anesthetics, myocardial ischemia, and alterations in loading conditions may cause errors in measurements, limiting the usefulness of bioimpedance cardiac output measurement in patients with coronary artery disease and impaired ventricular function. Changes in lead placement or changes in tissue water content, as seen in fluid shifts and pulmonary edema, may interfere with the signal. Bioimpedance systems have little control over the percentage of current passing through the vascular structures as the electrical impedance of the lungs changes with respiration, thus varying the total current passing through blood-containing structures. Bioimpedance systems are not reliable in patients after cardiopulmonary bypass, kidney transplants, congestive heart failure, pulmonary edema, sepsis, pregnancy, abdominal surgery, or critical illness.58–64 A novel system for the measurement of CO based on bioimpedance, called the endotracheal cardiac output monitor (ECOM), has also been assessed. It provides a continuous measurement of CO derived from impedance measurements from electrodes on the balloon and on the shaft of an endotracheal

86

tube. The shaft electrode serves as a ground. The field current is produced between the balloon electrode and the ground electrode on the tube. Orthogonal pairs of sensing electrodes on the balloon are used to measure the impedance signals.65 Thoracic electrical bioimpedance has been evaluated and compared with TDCO. CO values measured were reported equivalent to TDCO-derived values.66,67

Systems based on Doppler ultrasound High-frequency sound waves easily penetrate skin and other body tissues. On encountering tissues of different acoustic density, a fraction of an emitted ultrasound signal is reflected.68 When a sound beam is directed to a moving object, such as blood, the reflected sound wave changes its frequency (Doppler shift). The magnitude of this shift is directly proportional to the velocity of blood flow. Mathematically it is expressed as Fd = 2fo/C × V × cos␪, where Fd represents the Doppler shift, fo is the transmitted frequency, C is the velocity of ultrasound in blood (constant), V is the velocity of the moving blood, and cos␪ is the cosine of the angle between the direction of the moving blood and the transmitted ultrasound beam.69 Stroke volume can be calculated by multiplying the average blood velocity during a systolic cycle by the ejection time (stroke distance) and by the crosssectional area through which blood flows.70 Doppler signals can be obtained with an ultrasound probe placed externally at the suprasternal notch directed at the ascending aorta, at the tip of an endotracheal tube, or at the tip of an esophageal probe directed at the descending thoracic aorta. To measure peak velocity blood flow in the ascending aortic or pulmonary artery with surface ultrasound, the transducer is positioned either in the left parasternal position to measure transpulmonary blood flow or the suprasternal position to measure transaortic blood flow. The ultrasound beam should be transmitted parallel to the direction of blood flow; only angles up to 20◦ are clinically acceptable for measurements of blood velocity and, consequently, of CO. The cross-sectional area of the aorta can be determined by two-dimensional or M-mode echocardiography but more commonly is derived from a nomogram stored in the computer based on age, sex, height, and weight. There is 5 percent to 17 percent variation in the crosssectional area of the aorta between systole and diastole; this can introduce error in calculations. Although nomograms may correlate well in large population studies, they may be invalid for an individual patient.71 The USCOM ultrasonic cardiac output monitor (USCOM Pty Ltd; Coffs Harbour, NSW, Australia) is a commercially available device that measures cardiac output transcutaneously using such a transducer, based on continuous-wave Doppler ultrasound. It is more accurate than pulsed Doppler at higher velocities and does not need to obtain a two-dimensional image of the heart/outflow tract and accurate selection of a sample area.72

Chapter 8 – Cardiac Output and Intravascular Volume

Figure 8.7. Esophageal Doppler. The esophageal Doppler probe remains stable in the esophageal lumen and is positioned to maximize descending aortic flow signals.

Esophageal Doppler monitoring offers the advantages of the probe being in close proximity of the descending aorta, thus providing an excellent window for obtaining Doppler signals (Figure 8.7). A correction factor (K-factor) is incorporated in the equation to account for blood flow distributed to the head and upper extremities, but this itself may introduce a source of error in the measurement of CO, as it can fluctuate during surgery as a response to changes in sympathetic tone, arterial blood pressure, and alterations in anesthetic depth.73,74 Esophageal probes are available that allow near-simultaneous measurement of the velocity of the descending aortic flow and the descending aortic diameter. Transtracheal Doppler monitoring uses a pulsed Doppler probe transducer mounted on the tip of a standard endotracheal tube to obtain the aortic diameter and measure the Doppler shift of the ultrasound beam reflected by the blood in the ascending aorta. The patient’s trachea is intubated with a Doppler Tube (Applied Biometrics; Minetonka, MN); Doppler flow signals and visual representation of forward and reverse flow are used for optimum positioning of the transducer. The angle between the vector of the ultrasound signal and the direction of blood flow is used to calculate both the aortic diameter and blood velocity; this angle is assumed to be constant. Similarly, the aortic diameter is assumed to be constant throughout the cardiac cycle.75 Transesophageal echocardiography (TEE) is an essential perioperative diagnostic and monitoring tool; it is widely used to assess cardiac anatomy, left ventricular function, preload, myocardial ischemia, and cardiac valve function and repair. With TEE, CO can be derived by measurement of flow through a cardiac valve (most commonly, the mitral or aortic valve), left ventricular outflow tract, or main pulmonary artery. Perrino and colleagues have described a single transducer probe position to monitor left ventricular regional/global wall motion and also measure CO, with minimal positioning adjustments.76

The TEE probe is positioned to obtain a transverse plane, transgastric short-axis view of the left ventricle at the midpapillary level. By rotating the imaging array to approximately 120◦ , the left ventricular outflow tract and ascending aorta can be imaged lying parallel to the ultrasound beam, and aortic blood flow velocities measured by a continuous-wave Doppler beam focused at the level of the aortic valve. The aortic valve area is measured by planimetry. The CO may also be calculated by calculating the stroke volume, from the end-diastolic and endsystolic volume, and multiplying it by the heart rate. The USCOM device has been found to be reliable, on evaluation in animal experiments and clinical trials.72,77,78 Clinical trials using esophageal Doppler devices have given inconsistent results, probably because the techniques are operatordependent and need frequent manipulation of the probe.74,79 A comparison of various modalities available to measure CO are presented in Table 8.1.

Parameters monitored The parameters monitored by the different CO monitoring modalities are tabulated in Table 8.2. The TDCO-based systems (the most practical dye dilutionbased systems) are capable of measuring and deriving, with help of specialized PAC catheters and monitoring computers, the following parameters or indices continuously or intermittently: CO; central venous pressure; pulmonary artery pressure; pulmonary artery occlusion pressure; systemic vascular resistance and index; pulmonary vascular resistance and index; left/right ventricular stroke work index; right ventricular stroke volume and index; right ventricular end-diastolic volume and index; right ventricular end-systolic volume and index; right ventricular stroke volume and index; and right ventricular ejection fraction. In addition, the computer can derive the global enddiastolic volume, intrathoracic volume, and extravascular lung water from the collected data. The thermoindicator injectate disperses volumetrically and thermally within the pulmonary and cardiac volumes. The volume of distribution is termed the intrathoracic thermal volume, which is the sum of the intrathoracic blood volume and extravascular lung water. The intrathoracic blood volume comprises the end-diastolic volumes of all four cardiac chambers (global end-diastolic volume) and the pulmonary blood volume. The pulse contour analysis-based systems are capable of measuring and deriving the pulse-continuous CO, systemic vascular resistance, stroke volume variation, and pulse pressure variation, apart from arterial pressure and heart rate. Aside from these parameters, the systems needing TDCO with calibration also reflect global end-diastolic volume, intrathoracic volume, and extravascular lung water derived from the TDCO data. However, these parameters are not measured in real time. The electrical impedance cardiography-based systems calculate CO from the stroke volume and heart rate. They can also measure thoracic fluid content, left ventricular ejection time, systemic vascular resistance, and left cardiac work index.

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Monitoring in Anesthesia and Perioperative Care

Table 8.1.

Comparison of various modalities of measuring cardiac output

Degree of Invasiveness

Arterial cannulation

Calibration by another method required

Direct Fick’s Differential carbon dioxide partial rebreathing Dye dilution

Face mask Endotracheal tube/face mask

No No

No No

No Yes

Experimental Measures only CO

Central vein

Yes

No

No

Intermittent TDCO

Pulmonary artery

No

No

No

Continuous TDCO

Pulmonary artery

No

No

Yes

Repeated measurements not possible Clinical gold standard Special catheters available for mixed venous oximetry and end-diastolic volume estimation in addition

Diastolic contour Systolic contour

Yes Yes

Yes Yes

Yes Yes

Pulse pressure

Pulmonary artery Pulmonary artery/central vein Pulmonary artery∗

Yes

Yes∗

Yes

Modelflow

Pulmonary artery

Yes

Yes

Yes

Pressure recording analytical method Thoracic Endotracheal Esophageal Transtracheal TEE

No

Yes

No

Yes

No Endotracheal tube Esophageal No Esophageal

No No No No No

No No No No No

Yes Yes No Yes No

System

Technique

Fick’s principle

Indicator dilution

Pulse contour

Electric impedance cardiography Doppler ultrasound

Table 8.2.

Cardiac performance–related Continuous cardiac output Pulmonary artery pressures Left/right ventricular stroke work/volume Systemic/pulmonary vascular resistance Intravascular volume related Central venous pressure Global end-diastolic volume Intrathoracic volume Extravascular lung water Stroke volume/pulse pressure variation Right ventricular end-diastolic volume Left ventricular end-diastolic area

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Remarks

∗ Lithium dilution to calibrate in LiDCO. No calibration in Flotrac Only trend monitoring if not calibrated

Cardiac performance– and intravascular volume–related parameters measured by the different cardiac output techniques

Parameter

∗

Continuous real-time

Differential CO2 partial rebreathing

Thermodilution cardiac output

Arterial pulse contour analysis

Electrical impedance cardiography

Doppler ultrasound

Yes No No

Yes Yes Yes

Yes No Yes

Yes No Yes

Yes No Yes

No

Yes

Yes

Yes

No

No No No No No

Yes Yes Yes Yes No

No Yes∗ Yes∗ Yes∗ Yes

No Yes Yes Yes No

No No No No Yes

No

Yes

No

No

Yes

No

No

No

No

Yes

Parameters measured not in real-time but only during calibration, using thermodilution technique.

Chapter 8 – Cardiac Output and Intravascular Volume

Measurements of most real-time Doppler ultrasound-based systems are limited to cardiac output; they give no indication of other hemodynamic variables, such as pressure measurements, vascular resistance, or stroke work calculations. TEE monitoring provides multiple data apart from cardiac output and intravascular-related parameters but has the disadvantage of not being a continuous real-time monitor. The left ventricular end-diastolic area index can be estimated by TEE, which is a sensitive parameter for intravascular volume assessment.

Evidence of utility Clinically, CO should be measured in patients with unstable cardio–circulatory status and those dependent on the administration of catecholamines. The measured CO and the derived values serve as the basis for therapeutic decisions. If such decisions are made based on incorrect information, the result may prove fatal for the patient.80 A number of studies in critical care have shown the unreliability of clinical and radiological signs to evaluate hemodynamic status.81,82 The value of more comprehensive cardiovascular monitoring, especially with new noninvasive devices for estimating CO, is well documented.1,83 There is sufficient evidence to show that CO monitoring-directed hemodynamic management is beneficial, at least in patients at risk of – rather than having – established organ failure, such as high-risk surgical patients.84 The outcome benefit from hemodynamic manipulation using either invasive or noninvasive monitoring techniques has been demonstrated in high-risk surgery, severe heart failure, and sepsis.85–88 However, few studies have demonstrated outcome benefit in critically ill patients in whom metabolic, inflammatory, and cellular processes are often too far advanced for benefit to be gained from hemodynamic manipulations that prevent and/or reverse tissue hypoxia.84,89 A study in patients in cardiogenic shock also found that the PAC provided hemodynamic information that cannot be obtained by clinical evaluation.90 A landmark study by Connors and coworkers91 in the mid1990s suggested a rise in mortality rates in patients receiving a Swan-Ganz catheter, leading to a call for a moratorium on the catheter’s use.92 The outcomes of this study were later questioned, as most ICUs during that period had adopted Shoemaker’s “supra-normalized oxygen delivery philosophy” to raise the cardiac index and oxygen delivery and consumption by fluid loading and dobutamine infusion.85 This led to the calling of a Pulmonary Artery Catheter Consensus Conference, which reaffirmed the likely worth of the PAC and acknowledged the lack of conclusive data showing benefit or harm.93 The role of the PAC in improving outcome and reducing mortality and morbidity still remains under a cloud, with several large published studies (in critically ill patients, high-risk surgical patients, patients with lung injury, and heart failure patients) showing either no benefit or actual harm with the use of the PAC.94–97 A meta-analysis of 13 studies, including more than 5000 critically ill patients, recently concluded that

the use of the PAC is not associated with improved survival or reduced hospitalization.98

Putting it all together Accurate assessment of the intravascular status is important to improve patient outcomes, especially in the critically ill. Recent guidelines for the hemodynamic management of critically ill patients have emphasized the importance of adequate volume resuscitation in predicting favorable outcomes.3,99,100 Only 40 percent to 72 percent of ICU patients with hemodynamic instability are able to respond to fluid loading by a significant increase in stroke volume or CO, emphasizing the need for predictive factors to select patients who might benefit from volume expansion and to avoid ineffective, or even deleterious, volume expansion.3,101,102 A number of studies in surgical and medical intensive care and cardiac surgical patients, using pulse contour analysis–based systems, have consistently demonstrated that the magnitude of respiratory variation of surrogates of stroke volume allows accurate prediction of fluid responsiveness.103–106 When comparing evidence on dynamic measurements of fluid responsiveness, pulse contour analysis remains the simplest and the most accurate way to predict response to a fluid challenge.102 Automatic real-time monitoring of pulse pressure variation using pulse contour analysis-based systems allows a beat-to-beat measurement of left ventricular stroke volume and quantification of its variation during a short period of a few seconds.107 Monitoring and minimizing pulse pressure variation by volume loading during high-risk surgery improves postoperative outcome and decreases the length of hospital stay.108 Doppler recording of aortic blood flow also has been used to quantify the respiratory variation in aortic peak velocity or in velocity time integral at the level of the aortic annulus or in the descending aorta.109 In cardiac surgery, the esophageal Doppler ultrasoundbased system has been shown to assist in optimizing gut perfusion and to decrease perioperative complications.87 When used to guide intraoperative intravascular volume loading to optimize stroke volume in orthopedic surgery, it has been credited with a more rapid postoperative recovery and reducing hospital stay significantly.88 These studies, however, demonstrated greater sensitivity of stroke volume over CO, as compensatory tachycardia tended to maintain CO in the milieu of mild-to-moderate hypovolemia. Left ventricular end-diastolic area obtained using TEE has been demonstrated to be a reliable indicator of preload, but not of fluid responsiveness.

Complications Complications associated with CO monitoring are mostly related to the use of PAC and can be classified as those 1. Related to central venous access: unintentional trauma (to nearby vessels, pleura, and nerves) and air embolism.110 2. Related to catheterization procedure: transient dysrhythmias (usually during advance or withdrawal of the

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catheter), conduction blocks, knotting of PAC, and pulmonary artery trauma (most serious adverse effect, with an incidence of 0.1%–1.5% and associated with a 53% mortality rate).111,112 3. Related to catheter residence: venous/pulmonary thromboembolism/infarct, cardiac valve trauma, infection, and pulmonary artery rupture.113 4. Related to mismanagement: based on faulty data acquisition and incorrect interpretation.114 Complications with the pulse contour analysis-based systems are related to peripheral arterial cannulation and local infection/thromboembolism. Complications with devices, based on the indirect Fick’s principle, are airway-related. Complications with use of bioimpedence devices have not been reported. Complications with Doppler ultrasound devices are limited to devices involving insertion of esophageal probes. They are classified as 1. Probe-related: failure of introduction, thermal/pressure injuries of esophagus and vocal cords 2. Procedure-related: respiratory compromise (hypoxia, bronchospasm, laryngospasm), cardiovascular compromise (arrhythmia, hypotension, cardiac arrest, angina pectoris), infection, dysphagia, and nausea/vomiting

Credentialing The placement of a PAC and the correct interpretation of the CO and derived data from TDCO have a fairly long learning curve. The authors are not aware of any specific approved credentialing process for TDCO measurement; however, a few national bodies consider PAC insertion as a core procedural skill of an anesthesiologist. Pulse contour analysis-based systems have a short learning curve, as the devices are almost totally automated and little intervention is required. Accreditation activities are available for these devices with a contact process of one hour. Other minimally invasive techniques, such as the indirect Fick’s principle and the bioimpedance-based systems, are also automated and have short learning curves. CO measurement by TEE has a long learning curve. Certificate courses in basic and advanced conventional TEE are run by a number of professional bodies around the world. For example, an experience of six months of using TEE, after attending the basic course, has been described as minimal training for competence by the National Credentialing Committee of Malaysia. In the United States, there are several pathways to board certification in TEE. For anesthesiologists, board certification in perioperative TEE is most commonly achieved through serving a 12-month fellowship devoted to the anesthetic care of cardiothoracic surgical patients (i.e. a cardiac anesthesia fellowship). During this time, the trainee must receive specific training in TEE and must report a minimum of 300 intraoperative

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TEE exams (a minimum of 150 of which must be performed and personally reported by the trainee, and an additional 150 of which must be studied under appropriate supervision but not personally reported). In addition, the trainee must achieve a passing grade on an exam administered by the National Board of Echocardiography. All Doppler ultrasound-based systems are operatordependent and need frequent manipulation of the probe to obtain accurate data.115–117 Some instruction and practice are required to acquire the skill for Doppler ultrasound systems other than TEE, but this training time and cost is negligible compared with that of mastering conventional TEE.

Conclusions To date, PAC remains the primary clinical diagnostic and monitoring tool used to diagnose cardiac dysfunction and low cardiac output and to monitor their treatment. The accuracy and validity of the new modes of monitoring CO and measuring derived data, using less-invasive monitors based on the indirect Fick’s principle and arterial pulse contour analysis, bioimpedance, and Doppler ultrasound-based systems, has been elucidated. However, the technique used to validate the newer modes of CO has been TDCO, using PAC, an “imperfect gold standard,” which is often used imperfectly.84 In cardiac surgery, TDCO measurement, using PAC, remains the monitoring modality of choice, as other modes of CO measurement are erroneous in the presence of valvular regurgitation, shunts, balloon counterpulsation, and the like. The essential parameters monitored to guide therapy are CO, pulmonary artery pressures, pulmonary capillary wedge pressure, and the systemic/pulmonary vascular resistances. Computed parameters from the collected data help assess the cardiovascular status more comprehensively. In settings of intensive care and noncardiac surgery, use of minimally invasive devices, such as bioimpedance, pulse contour analysis, and Doppler ultrasound-based systems, is preferable, as real-time trends, rather than absolute values, have more value in guiding therapy. These devices dynamically assess the intravascular volume status. To predict fluid responsiveness in critically ill patients, dynamic parameters should be used preferentially to static parameters. The dynamic parameters that predict fluid responsiveness best are stroke volume variation and pulse pressure variation.

References 1. Dueck R. Noninvasive cardiac output monitoring. Chest 2001;120:339–40. 2. Pinsky MR, Teboul JL. Assessment of indices of preload and volume responsiveness. Curr Opin Crit Care 2005;11:235–9. 3. Michard F, Teboul JL. Predicting fluid responsiveness in ICU patients. A critical analysis of the evidence. Chest 2002;121:2000–8. 4. Kumar A, Anel R, Bunnell E, Habet K, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response

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42. Jansen JRC, Schreuder JJ, Mulier JP, Smith NT, Settels JJ, Wesseling KH. A comparison of cardiac output derived from the arterial pressure wave against thermodilution in cardiac surgery patients. Br J Anaesth 2001;87:212–22. 43. Langewouters GJ, Wesseling KH, Goedhard WJ. The pressuredependant dynamic elasticity of 35 thoracic and 16 abdominal human aortas invitro described by a five component model. J Biomech 1985;18:613–20. 44. Langewouters GJ, Wesseling KH, Goedhard WJ. The static elastic properties of 45 human thoracic and 20 abdominal aortas in vitro and the parameters of a new model. J Biomech 1984;17:425–35. 45. Remmen JJ, Aengevaeren WR, Verheugt FW, et al. Finapres arterial pulse wave analysis with Modelflow is not a reliable noninvasive method for assessment of cardiac output. Clin Sci (Lond) 2002;103:143–9. 46. Azabji Kenfack M, Lador F, Licker M, et al. Cardiac output by Modelflow method from intra-arterial and fingertip pulse pressure profiles. Clin Sci (Lond) 2004;106:365–9. 47. Tam E, Azabji Kenfack M, Cautero M, et al. Correction of cardiac output obtained by Modelflow from finger pulse pressure profiles with a respiratory method in humans. Clin Sci (Lond) 2004;106:371–6. 48. de Vaal JB, de Wilde RBP, Van Den Berg PCM, Schreuder JJ, Jansen JRC. Less invasive determination of cardiac output from the arterial pressure by aortic diameter-calibrated pulse contour. Br J Anaesth 2005;95:26–31. 49. Rhodes A, Sunderland R. Arterial pulse power analysis, the LiDCOTM plus system. In Pinsky MR, Pyen D, eds. Functional Hemodynamics. Berlin: Springer Verlag, 2005, pp. 183–92. 50. Button D, Weibel L, Reuthebuch O, Genoni M, Zollinger A, Hofer CK. Clinical evaluation of the FloTrac/VigileoTM system and two established continuous cardiac output monitoring devices in patients undergoing cardiac surgery. Br J Anaesth 2007; 99:329–36. 51. Chakravarthy M, Patil TA, Jayaprakash K, Kalligudd P, Prabhakumar D, Jawali V. Comparison of simultaneous estimation of cardiac output by four techniques in patients undergoing off-pump coronary artery bypass surgery – a prospective observational study. Ann Card Anaesth 2007;10:121–6. 52. Della Rocca G, Costa MG, Chiarandini P, et al. Arterial pulse cardiac output agreement with thermodilution in patients in hyperdynamic conditions. J Cardiothorac Vasc Anesth 2008;22:681–7. 53. Lorsomradee S, Lorsomradee S, Cromheecke S, De Hert SG. Uncalibrated arterial pulse contour analysis versus continuous thermodilution technique: effects of alterations in arterial waveform. J Cardiothorac Vasc Anesth 2007;21:636–43. 54. Breukers RMBGE, Sepehrkhouy S, Spiegelenberg SR, Groeneveld ABJ. Cardiac output measured by a new arterial pressure waveform analysis method without calibration compared with thermodilution after cardiac surgery. J Cardiothorac Vasc Anesth 2007;21:632–5. 55. Scolletta S, Romano SM, Biagioli B, Capannini G, Giomarelli P. Pressure recording analytical method (PRAM) for measurement of cardiac output during various haemodynamic states. Br J Anaesth 2005;95:159–65. 56. Kubicek WG. Development and evaluation of an impedance cardiac output system. Aerospace Med 1966;12:1208–12. 57. Sramek B. Cardiac output by impedance. Med Electronics 1982;4:93–7.

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58. Atallah MM, Demain AD. Cardiac output measurement. Lack of agreement between thermodilution and thoracic electric bioimpedance in two clinical settings. J Clin Anesth 1995;7:182–5. 59. Young JD, McQuillan P. Comparison of thoracic electrical bioimpedance and thermodilution for the measurement of cardiac index in patients with severe sepsis. Br J Anaesth 1993;70:58–62. 60. Weiss S, Calloway E, Cairo J, Granger W, Winslow J. Comparison of cardiac output measurements by thermodilution and thoracic electrical bioimpedance in critically ill versus non-critically ill patients. Am J Emerg Med 1995; 13:626–31. 61. Critchley LA, Critchley JA. Lung fluid and impedance cardiography. Anaesthesia 1998; 53:369–72. 62. Easterling TR, Benedetti TJ, Carlson KL, Watts DH. Measurement of cardiac output in pregnancy by thermodilution and impedance techniques. Br J Obstet Gynaecol 1989;96: 67–9. 63. Weiss SJ, Kulik JP, Calloway E. Bioimpedance cardiac output measurements in patients with presumed congestive heart failure. Acad Emerg Med 1997;4:568–73. 64. Critchley LA, Leung DH, Short TG. Abdominal surgery alters the calibration of bioimpedance cardiac output measurement. Int J Clin Monit Comput 1996; 13:1–8. 65. Wallace AW, Salahieh A, Lawrence A, Spector K, Owens C, Alonso D. Endotracheal cardiac output monitor. Anesthesiology 2000; 92:178–89. 66. Spiess BD, Patel MA, Soltow LO, Wright IH. Comparison of bioimpedance versus thermodilution cardiac output during cardiac surgery: evaluation of a second-generation bioimpedance device. J Cardiothorac Vasc Anesth 2001;15:567–73. 67. Sageman WS, Riffenburgh RH, Spiess BD. Equivalence of bioimpedance and thermodilution in measuring cardiac index after cardiac surgery. J Cardiothorac Vasc Anesth 2002;16: 8–14. 68. Bein B, Worthmann F, Tonner PH, et al. Comparison of esophageal Doppler, pulse contour analysis and realtime pulmonary artery thermodilution for the continuous measurement of cardiac output. J Cardiothorac Vasc Anaesth 2004;18:185–9. 69. Singer M, Bennet ED. Noninvasive optimization of left ventricular filling using esophageal Doppler. Crit Care Med 1991;19:1132–7. 70. Cheung AT, Savino JS, Weiss SJ, Aukburg SJ, Berlin JA. Echocardiographic and hemodynamic indexes of left ventricular preload in patients with normal and abnormal ventricular function. Anesthesiology 1994;81:376–87. 71. Perrino AC Jr. Cardiac output monitoring by echocardiography: Should we pass on Swan-Ganz catheters? Yale J Biol Med 1993;66:397–413. 72. Tan HL, Pinder M, Parsons R, Roberts B and van Heerden PV. Clinical evaluation of USCOM ultrasonic cardiac output monitor in cardiac surgical patients in intensive care unit. Br J Anaesth 2005;94:287–91. 73. List W, Gravenstein N, Banner T, et al. Interaction in sheep between mean arterial pressure and cross-sectional area of the descending aorta: implications for esophageal monitoring. Anesthesiology 1987;67:A178. 74. Perrino AC, Fleming J, LaMantia KR. Transesophageal cardiac output monitoring: Performance during aortic reconstructive surgery. Anesth Analg 1991;73:705–10.

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75. Seigel LC, Fitzgerald DC, Engstom RH. Simultaneous intraoperative measurement of cardiac output by thermodilution and transtracheal Doppler. Anesthesiology 1991;74:664–9. 76. Perrino AC, Harris SN, Luther MA. Intraoperative determination of cardiac output using multiplane transesophageal echocardiography: a comparison to thermodilution. Anesthesiology 1998;89:350–357. 77. Critchley LA, Peng ZY, Fok BS, Lee A, Phillips RA. Testing the reliability of a new ultrasonic cardiac cutput monitor, the USCOM, by using aortic flowprobes in anesthetized dogs. Anesth Analg 2005;100:748–53. 78. Phillips RA. Transcutaneous continuous-wave Doppler monitoring is feasible producing reliable and reproducible signals. J Am Coll Cardiol 2002; 39(Suppl B):283. 79. Spahn DR, Schmid ER, Tornic M, et al. Noninvasive versus invasive assessment of cardiac output after cardiac surgery: clinical validation. J Cardiothorac Anesth 1990;4:46–59. 80. Zimmermann A, Kufner C, Hofbauer S, et al. The accuracy of the Vigileo/FloTrac continuous cardiac output monitor. J Cardiothorac Vasc Anesth 2008;22:388–93 81. Eisenberg PR, Jaffe AS, Schuster DP. Clinical evaluation compared to pulmonary artery catheterisation in the haemodynamic assessment of critically-ill patients. Crit Care Med 1984;12:549–53 82. Bayliss J, Norell M, Ryan A, et al. Bedside haemodynamic monitoring: experience in a general hospital. Br Med J 1983;287:187–90. 83. Gan TJ, Soppitt A, Maroof M, et al. Goal-directed intraoperative fluid administration reduces length of hospital stay after major surgery. Anesthesiology 2002;97:820–826. 84. Singer M. Cardiac output in 1998. Heart 1998;79:425–8. 85. Shoemaker WC, Appel PL, Kram HB, et al. Prospective trial of supranormal values of survivors as therapeutic goals in high-risk surgical patients. Chest 1988;94:1176–86. 86. Boyd O, Grounds RM, Bennett ED. A randomized clinical trial of the effect of deliberate perioperative increase of oxygen delivery on mortality in high-risk surgical patients. JAMA 1993;270:2699–707. 87. Mythen MG, Webb AR. Peroperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion in cardiac surgery. Arch Surg 1995;130:423–9. 88. Sinclair S, James S, Singer M. Intraoperative intravascular volume optimisation and length of hospital stay after repair of proximal femoral fracture: randomised, controlled trial. BMJ 1997;315:909–12. 89. Mimoz O, Rauss A, Rekik N, et al. Pulmonary artery catheterization in critically ill patients: a prospective analysis of outcome changes associated with catheter-prompted changes in therapy. Crit Care Med 1994;22:573–9. 90. Linton RAF, Linton NWF, Kelly F. Is clinical assessment of the circulation reliable in postoperative cardiac surgical patients? J Cardiothorac Vasc Anesth 2002;16:4–7. 91. Connors AF Jr, Speroff T, Dawson NV, et al. The effectiveness of right heart catheterization in the initial care of critically ill patients. SUPPORT Investigators. JAMA 1996;276:889–97. 92. Dalen JE, Bone RC. Is it time to pull the pulmonary artery catheter? JAMA 1996;276:916–18. 93 Pulmonary artery catheter consensus conference: consensus statement. Crit Care Med 1997;25:910–25. 94. Harvey S, Harrison DA, Singer M, et al. Assessment of the clinical effectiveness of pulmonary artery catheters in

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Chapter

9

Gastric tonometry Elliott Bennett-Guerrero

Background The gut is one of the most susceptible organs to hypoperfusion during conditions of trauma or stress.1–3 More than three decades ago, Price and colleagues removed 15 percent of the blood volume from healthy volunteers, causing a 40 percent reduction in splanchnic blood volume.2 In this study, cardiac output (CO), blood pressure (BP), and heart rate (HR) did not change from baseline. A more recent study was conducted by Hamilton-Davies and associates, in which 25 percent of the blood volume was removed from six healthy volunteers.4 Gastric mucosal perfusion, as measured by saline gastric tonometry, was the first variable to decline (in five of the six subjects). Stroke volume (SV) also decreased; however, routinely measured cardiovascular variables such as HR, BP, and CO did not change significantly enough from baseline values to cause suspicion of a hypovolemic state. These studies suggest that during periods of hypovolemia, the gut vasoconstricts, thus shunting blood toward “more vital organs,” such as the heart and brain.1–3 Gut hypoperfusion can progress to ischemia, which may result in complications that take place many hours and days following an episode of hypovolemia.5

Technical concepts Until recently, an FDA-approved monitor (the gastrointestinal tonometer) was available to measure gut hypoperfusion (Tonocap; GE Healthcare, Barrington, IL). The tonometer is a naso/orogastric tube that is modified to include a silicone balloon into which air or saline is introduced (Figure 9.1). The most recent commercially available method of tonometry involved the introduction of air into the tonometer’s balloon. Following a brief period of equilibration (⬍15 minutes), air in the balloon is assayed for PCO2 by the monitor’s accompanying infrared analyzer. This newer method allowed for the determination of gastric mucosal PCO2 every five minutes. The gastric mucosal bed is similar to the overall splanchnic mucosa in its propensity to become hypoperfused during periods of physiologic stress. Hypoperfused areas of tissue develop regional hypercapnia (elevated PCO2 ), which diffuses into the tonometer balloon, allowing for an indirect measurement of gastric mucosal PCO2 . Hypoperfusion is manifested by a positive gap between the gastric mucosal PCO2 and the arterial

PCO2 (gastric mucosal PCO2 ⬎ arterial PCO2 ). A gap greater than 8 mmHg is considered to reflect splanchnic hypoperfusion.6 In theory, any gap is abnormal; however, the use of a higher cutoff value appears to improve the specificity of this monitor without significantly decreasing its sensitivity. Initially, early studies reported “pHi,” which is a calculated measure that takes into account both the level of CO2 in the stomach and the plasma bicarbonate concentration. However, Schlichtig and colleagues correctly reported that the gastric– arterial PCO2 difference is a better and more specific measure of gastric ischemia, because pHi can be low in the setting of a metabolic acidosis even if gastric PCO2 is not elevated.7

Evidence of utility Observational studies Several studies have observed a high incidence of splanchnic hypoperfusion during cardiac surgery, with some showing an association between abnormal gut perfusion during cardiac surgery and postoperative complications.8–15 Fiddian-Green and Baker used saline tonometry to measure gastric mucosal perfusion in 85 cardiac surgical patients.11 Half (49%) of these patients developed evidence of abnormal perfusion, and all serious postoperative complications (eight patients, including five deaths) developed in this group. Gastric tonometry was shown in this and in other studies to be a more sensitive predictor of adverse postoperative outcome compared with more routinely used global measures such as CO, BP, HR, and urine output.12, 14 Several studies have demonstrated an association between gastric ischemia, as manifested by elevated gastric PCO2 , and adverse outcome after routine elective cardiac surgery.14,15 Studies that have failed to demonstrate an association between splanchnic hypoperfusion and adverse postoperative outcome are limited in part by small sample size, insensitive measures of postoperative morbidity, and deviation from validated methodology of tonometry.9,10 In addition, tonometric measurements of gastric mucosal perfusion during hypothermic cardiopulmonary bypass (CPB) have not been validated in terms of their ability to predict postoperative morbidity. In addition to studies involving cardiac surgery, there are several observational studies showing an association between

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Credentialing

Gastric muscularis Arterial blood supply Gastric mucosa

-

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H+ + HCO3-

CO2 H2CO3

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16-French gastric catheter for drainage and feeding Tonometer balloon

Figure 9.1. Diagram of operation of gastric tonometer in gastric lumen. Tonometer balloon is filled with either saline solution or air. Protons (H+ ) are generated in the gastric mucosa from anaerobic metabolism (tissue acidosis). Protons then combine with bicarbonate (HCO– 3 ) to form carbonic acid (H2 CO3 ), which dissociates into carbon dioxide (CO2 ) and water (H2 O). Carbon dioxide diffuses freely into the gastric lumen and tonometer balloon.

abnormal tonometric variables and adverse outcome in ICU,16 trauma,17 and noncardiac surgical patients.18

Randomized clinical trials Observational studies cannot prove that the use of the monitor “causes” or results in better outcome. Unfortunately, there are few published randomized clinical trials of gastric-tonometry– guided care versus the standard-of-care therapy. Gutierrez and associates randomized ICU patients to standard of care versus gastric-tonometric–guided care, in which apparent splanchnic ischemia was treated with strategies aimed at optimizing oxygen delivery.19 For patients who were admitted to the ICU with normal pHi (no apparent ischemia), those randomized to the tonometric-guided care exhibited higher survival (58% vs 42%; p ⬍ 0.01). In contrast, for patients with evidence of gastric ischemia on admission to the ICU, there was no apparent benefit to this experimental intervention (survival 37% vs 36%). Ivatury and coworkers randomized ICU patients to gastrictonometric–guided care versus maintenance of oxygen delivery.20 There was no apparent benefit to the tonometric-guided care, although the comparison group was not a true standardof-care group. The study did, however, show an association between splanchnic ischemia using tonometry and adverse outcomes consistent with previous studies. Therefore, at the current time, there are scant data from randomized clinical trials to address the question of whether gastric tonometry can be used to improve outcome.

Complications Gastric tonometry is minimally invasive and carries few risks. It should not be used in patients for whom instrumentation of the stomach or esophagus would be contraindicated.

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Gastric tonometry is not currently available; however, no specific credentialing process or training have been required.

Practice parameters Gastric tonometry is not currently available. There is a large body of observational studies that provide a theoretical justification for its use, but there are scant data from randomized clinical trials, so its use cannot be strongly recommended at this time.

References 1. Mythen MG, Webb AR. The role of gut mucosal hypoperfusion in the pathogenesis of post-operative organ dysfunction. Intensive Care Med 1994;20:203–9. 2. Price HL, Deutsch S, Marshall BE, Stephen GW, Behar MG, Neufeld GR. Hemodynamic and metabolic effects of hemorrhage in man, with particular reference to the splanchnic circulation. Circ Res 1966;18:469–74. 3. Lundgren O. Physiology of intestinal circulation. In Martson A, et al., eds. Splanchnic Ischemia and Multiple Organ Failure. St. Louis: Mosby, 1989, pp. 29–40. 4. Hamilton-Davies C, Mythen MG, Salmon JB, Jacobson D, Shukla A, Webb AR. Comparison of commonly used clinical indicators of hypovolaemia with gastrointestinal tonometry. Intensive Care Med 1997;23:276–81. 5. Fink MP. Effect of critical illness on microbial translocation and gastrointestinal mucosa permeability. Semin Respir Infect 1994;9:256–60. 6. Mythen MG, Faehnrich J. Monitoring gut perfusion. In Rombeau JL, Takala J, eds. Gut Dysfunction in Critical Illness. Heidelberg: Springer-Verlag, 1996, pp. 246–63. 7. Schlichtig R, Mehta N, Gayowski TJ. Tissue-arterial PCO2 difference is a better marker of ischemia than intramural pH (pHi) or arterial pH-pHi difference. J Crit Care 1996;11:51–6. 8. Berendes E, Mollhoff T, Van Aken H, et al. Effects of dopexamine on creatinine clearance, systemic inflammation, and splanchnic oxygenation in patients undergoing coronary artery bypass grafting. Anesth Analg 1997;84:950–7. 9. Andersen LW, Landow L, Baek L, Jansen E, Baker S. Association between gastric intramucosal pH and splanchnic endotoxin, antibody to endotoxin, and tumor necrosis factor-alpha concentrations in patients undergoing cardiopulmonary bypass. Crit Care Med 1993;21:210–7. 10. Riddington DW, Venkatesh B, Boivin CM, et al. Intestinal permeability, gastric intramucosal pH, and systemic endotoxemia in patients undergoing cardiopulmonary bypass. JAMA 1996;275:1007–12. 11. Fiddian-Green RG, Baker S. Predictive value of the stomach wall pH for complications after cardiac operations: comparison with other monitoring. Crit Care Med 1987;15:153–6. 12. Mythen MG, Webb AR. Intra-operative gut mucosal hypoperfusion is associated with increased post-operative complications and cost. Intensive Care Med 1994;20:99–104. 13. Mythen MG, Webb AR. Perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion during cardiac surgery. Arch Surg 1995;130:423–9. 14. Bennett-Guerrero E, Panah MH, Bodian CA, et al. Automated detection of gastric luminal partial pressure of carbon dioxide

Chapter 9 – Gastric Tonometry

during cardiovascular surgery using the Tonocap. Anesthesiology 2000;92:38–45. 15. Kavarana MN, Frumento RJ, Hirsch AL, Oz MC, Lee DC, Bennett-Guerrero E. Gastric hypercarbia and adverse outcome after cardiac surgery. Intensive Care Med 2003;29:742–8. 16. Levy B, Gawalkiewicz P, Vallet B, Briancon S, Nace L, Bollaert PE. Gastric capnometry with air-automated tonometry predicts outcome in critically ill patients. Crit Care Med 2003;31:474–80. 17. Calvete JO, Schonhorst L, Moura DM, Friedman G. Acid-base disarrangement and gastric intramucosal acidosis predict outcome from major trauma. Rev Assoc Med Bras 2008;54: 116–21.

18. Lebuffe G, Vallet B, Takala J, et al. A European, multicenter, observational study to assess the value of gastric-to-end tidal PCO2 difference in predicting postoperative complications. Anesth Analg 2004;99:166–72. 19. Gutierrez G, Palizas F, Doglio G, et al. Gastric intramucosal pH as a therapeutic index of tissue oxygenation in critically ill patients. Lancet 1992;339:195–9. 20. Ivatury RR, Simon RJ, Islam S, Fueg A, Rohman M, Stahl WM. A prospective randomized study of end points of resuscitation after major trauma: global oxygen transport indices versus organ-specific gastric mucosal pH. J Am Coll Surg 1996;183:145–54.

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10

Oxygen delivery, oxygen transport, and tissue oxygen tension Critical monitoring in the ICU Jayashree Raikhelkar and Peter J. Papadakos

Introduction A continuous supply of oxygen is essential for aerobic metabolism and maintenance of natural functioning in all cells. When metabolic needs of an organ exceed supply, tissue and organ dysfunction result and a state of shock ensues. This overview focuses on the fundamental concepts of oxygen delivery (DO2 ) and utilization by tissues as well as special emphasis on monitoring of DO2 and tissue perfusion in the critically ill.

Oxygen transport and delivery variables Global DO2 is dependent on an intact respiratory system. Respiratory failure can lead to inadequate oxygen delivery, tissue hypoxia, and organ injury. The availability of oxygen to tissues can be quantified by a number of measured variables. The partial pressure of oxygen in the plasma (PaO2 ) and the arterial oxygen saturation (SaO2 ) are some of the principal components for assessment of adequacy of oxygen transport and delivery. Although regularly used to monitor respiratory function, PaO2 is largely dependent on ventilation/perfusion matching.1 PaO2 and SaO2 may be normal in cases of anemia and low cardiac output states. The alveolar PO2 -to-PaO2 gradient (A–a gradient) is a better indicator of integrity of oxygen transport from the alveoli to the blood.2 Arterial O2 content of blood is given as CaO2 = (1.39 × Hb × SaO2 ) + (0.0031 × PaO2 ), where CaO2 is the oxygen content of arterial blood and Hb is the hemoglobin concentration. The total concentration of oxygen in arterial blood in an average-sized adult is approximately 200mL per liter. More than 98 percent of this oxygen is bound to hemoglobin, and the remaining 1.5 percent is dissolved in the plasma. This underscores the significance of hemoglobin in the transport of oxygen within the body. The concentration of O2 in venous blood (CvO2 ) is calculated in a similar fashion to CaO2 , with the use of venous O2 saturation (SvO2 ) and PO2 (PvO2 ): CvO2 = (1.34 × Hb × SvO2 ) + (0.003 × PvO2 ). The rate at which oxygen is delivered to the peripheral tissues by cardiac output can be derived by the Fick equation: DO2 = 10 × Qt × CaO2 ,

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where Qt is cardiac output. DO2 is the volume of oxygen (mL) that reaches the peripheral capillary bed every minute. From the equation, one can easily deduce that the most effective way to increase global DO2 to the tissues is by increasing hemoglobin concentration and by secondarily increasing cardiac output (3). The plateau of the oxygen equilibrium curve (OEC) is attained at an oxygen saturation of 90 percent (Figure 10.1). Above this level, additional oxygen does not significantly enhance DO2 . Shifting of the ODC affects SaO2 and, consequently, DO2 . Shifts to the right occur with increased 2,3-diglycerophosphate, acidosis, and hyperthermia. In contrast, decreased 2,3diglycerophophate, alkalosis, and hypothermia shift the curve to the left, increasing hemoglobin saturation for any given PO2 . The rate at which delivered oxygen is metabolically consumed is oxygen uptake (VO2 ) and is presented in a variation of the Fick equation: VO2 = 10 × CO(CaO2 −CvO2 ). Further modified, the equation can be stated as: VO2 = Qt × 13.4 × Hb × (SaO2 −SvO2 ). The Fick equation does not take into oxygen consumption by the lung. Normal lung VO2 accounts for less than 5 percent of total VO2 . In the critically ill, this fraction may increase to up to 20 percent (4). Direct measurement of VO2 involves measurement of whole-body VO2 and is therefore a more accurate measurement of VO2 (5). Another important measure of oxygen transport is oxygen extraction ratio (O2 ER). It is defined as the fraction of oxygen delivered to the capillaries that is taken up by the tissues: O2 ER = VO2 /DO2 . Under resting conditions, 25 percent of the total oxygen delivered is extracted by the tissues. Individual organ O2 ERs vary, with metabolically active organs such as the heart and brain having higher values.

Critical DO2 In healthy individuals, as VO2 increases with physiologic stress, oxygen delivery will increase simultaneously. After a certain point, the O2 ER will increase to maintain oxygen delivery. Critical DO2 is the level of oxygen transport at which VO2 begins

Chapter 10 – Oxygen Delivery, Oxygen Transport, and Tissue Oxygen Tension

Figure 10.1. The hemoglobin–oxygen dissociation curve with factors known to increase and decrease hemoglobin’s affinity for oxygen.

Oxygen-hemoglobin dissociation curves 100% pH 7.60

90%

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uploading under the above conditions.

Decreased H (increased pH) Decreased CO2 Decreased temperature Decreased 2, 3-DPG Fetal hemoglobin Carbon monoxide poisoning

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Oxygen consumption (VO2’ mL/min)

to decline, becoming a supply-dependent variable (6) (Figure 10.2). In critical illness, there is a reduced ability for tissues to extract oxygen. As the slope of O2 ER continues to increase, oxygen debt and anaerobic glycolysis result and shock ensues (7, 8). Multiple clinical trials comparing optimum versus normal resuscitation endpoints in severely critically ill patients have been inconclusive. Velmahos and colleagues found no difference in the rate of death, organ failure, and ICU stay (9). Kern and associates’ meta-analysis evaluating hemodynamic goals in acute, critically ill patients and evaluation of outcomes of 300

Critical DO2

resuscitation therapy showed that optimization of hemodynamic variables prior to the onset of multiorgan failure significantly reduced mortality as compared with doing so after the onset of multisystemic dysfunction (10). Rivers and coworkers also concluded that early goal-directed therapy in cases of severe sepsis and septic shock results in less-severe organ failure (11,12). These studies may suggest that timely therapeutic intervention and optimization, not supranormalization of hemodynamic variables, is the key to successful management of shock and avoidance of multiorgan dysfunction. The normal ranges for oxygen transport variables are given in Table 10.1.

Monitoring of DO2 (global and regional) Metabolic indicators of tissue perfusion

200 Healthy subject

The assessment of intravascular volume and adequacy of resuscitation presents unique clinical challenges. Clinical indicators

100 Table 10.1.

Oxygen transport variables

Critically ill patient 0 0

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Oxygen delivery (DO2’ mL/min) Figure 10.2. Schematic representation of the relationship between DO2 and V_ O2 in healthy and critically ill individuals.2 ( Reproduced from reference. 3, with permission from BMJ Publishing Group Ltd.)

Parameters

Normal range (size-adjusted)

1. Oxygen delivery (DO2 ) 2. Oxygen uptake (VO2 ) 3. Oxygen extraction ratio (O2 ER) 4. Mixed venous oxygen saturation (SvO2 ) 5. Cardiac output (CO)

520–570 mL/min/m2 110–160 mL/min/m2 20%–30% 70%–75% 2.4–4.0 L/min/m2

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Glycolysis

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2 ATP

38 ATP

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CO2 + H2O

Pyruvate O2

concluded, however, that in patients with peak blood lactate levels greater or equal to 2.5 mmol/L, the anion gap is an insensitive screen for elevated lactate in a critically ill, hospitalized population (21). Fifty-seven percent of the patients with elevated lactate levels did not have an elevated anion gap, suggesting that hyperlactatemia should be included in the differential diagnosis of nonanion gap acidosis. Acidosis (pH ⬍7.30) was not found to alter mortality.

Anaerobic metabolism

Lactate Figure 10.3. Aerobic and anaerobic metabolic pathways.

of tissue perfusion have been extensively studied and used to guide resuscitative efforts in shock. Conventional markers, such as heart rate, blood pressure, and urine output, have been disappointing measures of ongoing tissue hypoxia (13) and have failed to predict diminished oxygen delivery or correlate with the various stages of shock (14). Serum lactate and base deficit have proved to be reliable indicators in resuscitation. These metabolic indicators of tissue perfusion are global measures of total body oxygen debt.

Serum lactate Abnormalities in lactate metabolism are a common occurrence in the critically ill and are a direct result of systemic hypoperfusion and ongoing tissue hypoxia. Lactate is a byproduct of anaerobic metabolism after glycolysis. At the tissue level, as a result of uncoupling of oxygen demands and supply, pyruvate cannot enter the Krebs cycle; instead, pyruvate is converted to lactate. If there continues to be an insufficient cellular oxygen supply, lactic acidosis ensues. Anaerobic glycolysis leads to the production of two molecules of adenosine triphosphate (ATP) per molecule of glucose, rather than 38 molecules of ATP from aerobic glycolysis (Figure 10.3). Initial serum lactate levels are normally used to direct resuscitative efforts and do correlate with mortality (15,16). The monitoring of lactate concentrations over time appears to be more predictive of mortality than monitoring of initial lactate concentrations. Multiple studies have indicated that the time required for clearance of lactate or normalization of lactate during resuscitation from shock can be used as an index of outcome (17–19). The use of lactate as a marker of tissue perfusion has limitations. Hyperlactatemia can be produced in type B lactic acidosis in the absence of tissue malperfusion. Also, for blood lactate levels to increase, lactate must accumulate and leak outside a tissue into the systemic circulation, and its rate of production must surpass its rate of uptake by other organs (20). The anion gap is a commonly used screening test for the presence of lactic acidosis. A study in surgical ICU patients

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Base deficit Base deficit is a derived variable, and is defined as the amount of additional base (mmol) required to normalize the pH of 1 L of whole blood. It is calculated from the blood gas analyzer from the PCO2 , pH, and HCO3 – values applied to a standard nomogram. Base deficit = −[(HCO3 ) − 24.8 + (16.2 × (pH − 7.4))] An elevated base deficit has been a proven marker of mortality from many studies, and has been shown to have direct correlation with lactate levels (22,23). The severity of this deficit has been directly linked to the volume of fluid replacement within the first 24 hours of resuscitation. Husain and colleagues reported that initial base deficit values are poor predictors of mortality and do not correlate with lactate levels in the surgical intensive care population (24). Base deficit measurements have proved usefulness in trauma populations. In a prospective observational study conducted by Schmelzer and associates (25), the measurement of central venous base deficit was predictive of survival past 24 hours. Paladino and colleagues concluded that the additional information derived from metabolic parameters such as lactate and base deficit with traditional vital signs increases the sensitivity of the ability to distinguish major and minor injury by 76 percent (26). Metabolic derangements, such as hyperchloremic acidosis from the administration of normal saline, renal failure, or diabetic ketoacidosis, can produce a metabolic acidosis distinct to tissue malperfusion and alter base deficit values. Furthermore, the administration of sodium bicarbonate can confound the utility of base deficit during resuscitation (27, 28).

Mixed venous oxygen saturation (SvO2) SvO2 measurement is considered a gold standard in determining adequacy of oxygen delivery and global tissue perfusion. Blood is aspirated from the distal port of a pulmonary artery catheter. It represents the saturation of blood returning to the pulmonary artery after mixing in the right ventricle. The formula for the SvO2 calculation can be derived by modification of the Fick equation: SvO2 = SaO2 −VO2 /CO × 1.34 × Hb A decrease in the SvO2 is indicative of a reduction in total oxygen delivery. This may include one or more of the following situations: (a) decreased CO; (b) increased oxygen consumption; (c) decreased arterial oxygen saturation; or (d) decreased

Chapter 10 – Oxygen Delivery, Oxygen Transport, and Tissue Oxygen Tension

hemoglobin concentration. Normal values range from 70 percent to 75 percent. SvO2 values below 60 percent may be a sign of cellular oxidative impairments; values consistently below 50 percent are indicative of anaerobic metabolism (29).

Central venous oxygen saturation (ScvO2) SvO2 is a very useful monitoring in the management of shock, but it requires the placement of PAC, which is less routinely used in modern day critical care. Recent literature has focused on the sampling of central venous oxygen saturation (ScvO2 ) in the resuscitation in septic shock with impressive results (12). ScvO2 is the oxygen saturation of venous blood measured near the junction of the superior vena cava and the right atrium. Advantages of ScvO2 sampling include the need for only a central venous catheter and its ability to be used for patients in whom a PAC cannot be inserted, such as in pediatric patients. ScvO2 values are usually less than the corresponding SvO2 by about 2percent to 3 percent because of the higher extraction ratio of the brain (30, 31). Much controversy has arisen regarding whether ScvO2 is an actual surrogate to SvO2 . The differences between the absolute values of ScvO2 and SvO2 changes with the degree of shock and the type of shock (32, 33). The SvO2 and ScvO2 parallel has been studied extensively. Yazigi and coworkers evaluated the correlation between the two in 64 consecutive postcardiac surgical patients. The study revealed a large discrepancy in ScvO2 and SvO2 values sampled. It was concluded that in patients after coronary artery surgery, ScvO2 could not be used as a direct alterative to SvO2 (34). Chawla and associates studied paired samplings of ScvO2 and SvO2 in a mixed medical and surgical population requiring a PAC to guide fluid therapy. They concluded that measurements of ScvO2 and SvO2 were not equivalent in this sample of critically ill patients and that ScvO2 was not a reliable surrogate for SvO2 (35). However, Dueck and colleagues recently performed a prospective clinical trial sampling ScvO2 and SvO2 measurements in patients undergoing elective neurosurgical procedures. In this sample of patients, the absolute values of ScvO2 were not equivalent to those of SvO2 in varying hemodynamic conditions, but the trend of ScvO2 may be substituted for the trend of SvO2 (36). Tahvanainen and coworkers found similar results (37). Further studies are required for evaluation and validation of ScvO2 during resuscitation for specific patient populations.

Regional indicators of tissue perfusion Regional endpoints are intended for the early detection of tissue ischemia and hypoxia in the microvasculature; when compared with global endpoints of resuscitation, they have been superior predictors of outcome (38).

Near-infrared spectroscopy Near-infrared spectroscopy (NIRS) has emerged in recent years as a potentially valuable way of monitoring hypoperfusion

noninvasively and optimizing oxygen delivery and consumption specifically at the tissue level. NIRS uses computer analysis of spectra in the near-infrared range, 700 nm to 2500 nm, to determine the oxidation state of hemoglobin in tissues. Light is absorbed by the various derivatives of hemoglobin, such as oxyhemoglobin (HbO2 ), deoxyhemoglobin (Hob), and myoglobin, which differ in near-infrared wavelengths (39). Tissue oxygen saturation (StO2 ) is calculated from an intricate algorithm of the ratio of absorption of wavelengths of the individual hemoglobins. This developing technology is allowing for swift, noninvasive approximation of local tissue oxygen saturation (40). McKinley and colleagues (41) compared changes in StO2 with a series of clinical indices of resuscitation in trauma patients. This study demonstrated changes in skeletal muscle StO2 paralleled oxygen delivery during the resuscitation of severely injured trauma patients who were at risk of developing multiple-organ failure. Multiple studies have been done with NIRS technology in patients with various degrees of sepsis. Measurements comparing muscle StO2 values in resuscitated sepsis patients and healthy volunteers were found to be inconsistent. In some studies, StO2 measurements between the two groups were found to be comparable (42, 43). Creteur and associates established that there are frequent alterations in muscle StO2 in a large population of critically ill sepsis patients and that these alterations are more prevalent in the presence of shock (44). Mulier and colleagues (45) concluded that NIRS measurements of StO2 correlated with invasive hemodynamic measurements in patients with severe sepsis but did not correlate with severity of illness. These findings suggest that NIRS may be clinically useful in measurement and monitoring of patients with severe sepsis. Additional studies are required for the evaluation of NIRS technology in the early resuscitation phase of sepsis. (See Chapter 21 for a more extensive discussion of NIRS.)

Tissue CO2 monitoring Tissue hypoperfusion in the gastrointestinal tract in the face of disturbed hemodynamics is well documented. Gastric tonometry and sublingual capnometry are based on the premise that tissue CO2 levels escalate in conditions in which gut tissue perfusion is impaired (46–48). CO2 is liberated when excess hydrogen ions are formed from the breakdown of high-energy phosphate compounds during tissue hypoperfusion, which are then buffered by bicarbonate (49). Gastric tonometric measurements of gastric intramucosal pH (pHi) correlate with splanchnic vascular blood flow, with pHi decreasing in value as splanchnic perfusion diminishes. Although pHi is the first to be affected during the onset of shock (50), it has been shown to correlate poorly with lactate and base deficit (51, 52). In the critical care arena, gastric tonometry has been used to titrate vasopressor agents to improve perfusion of the gastrointestinal tract in the critically ill (53, 54). Various studies have demonstrated its usefulness in predicting weaning outcomes in patients being

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BL

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Figure 10.4. Comparison of sublingual PCO2 (PslCO2 ), gastric PCO2 (PgCO2 ), and arterial lactate (LAC) before, during, and after reversal of hemorrhage. All values represent mean ± standard deviation. P ⬍ 0.05, ∗ p ⬍ 0.01 versus baseline. (From reference 59. Copyright American Thoracic Society.)

liberated from mechanical ventilation (55, 56). Limitations of gastric tonometry include the requirement of placement of specialized nasogastric tubes, excluding pediatric patients; slow calibration time; and the inability to provide enteral nutrition while measurements are being taken (49). (See Chapter 9 for a more complete description of gastric tonometry.) Sublingual capnometry, on the other hand, is an easily accessible method to evaluate perfusion of the splanchnic circulation. A sensor placed beneath the tongue measures the partial pressure of carbon dioxide (PslCO2 ) generated. Several studies have confirmed that an increase in sublingual PCO2 correlated with reductions in mean arterial pressure – and, thus, cardiac output – during hemorrhagic and septic shock (57–60). Nakagawa and colleagues investigated sublingual tissue PCO2 during hemorrhagic and septic shock in rats. In both forms of shock, highly significant linear correlations were observed among end-tidal PCO2 , sublingual PCO2 , and arterial blood lactate levels (Figure 10.4) (59). A PslCO2 value of 70 mmHg or more has been linked to elevated arterial lactate levels and is predictive of decreased hospital survival (61). Limitations of sublingual capnography include the fact that sublingual mucosa is not perfused by splanchnic blood flow; therefore, elevations in PslCO2 may be delayed compared with pHi levels in progressive shock states. Therefore, it may not serve as a “canary” of the body (62). Both Marik (63) and Rackow (64) found higher differences between PslCO2 and PaCO2 values (⌬ Psl–aCO2 ) in hemodynamically unstable nonsurvivors versus survivors admitted to the ICU. This suggests that ⌬ Psl-aCO2 is a better prognostic indicator than PslCO2 alone.

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Orthogonal polarization spectral (OPS) imaging employs polarized light to directly visualize the microcirculation. Polarized light is transmitted to hemoglobin molecules in the microcirculation, which in turn absorbs and reflects the light to a videomicroscope (65). The functional density of the capillaries imaged has been shown to be a sensitive marker of tissue perfusion (66). De Backer and coworkers reported that the density, as well as the total number, of sublingual vessels diminished significantly in patients with sepsis compared with controls (67). Other tissues evaluated with OPS imaging include oral, sublingual, rectal, and vaginal mucosa. Currently, OPS imaging remains an investigational method of monitoring (68).

Transcutaneous oxygen tension Direct measurements of oxygen and carbon dioxide tension within the skin with the help of heated probes is a monitoring modality that was first developed 30 years ago. In a state of shock, similar to the splanchnic circulation, the skin and skeletal muscle blood flow is restricted. Measurements of oxygen and carbon dioxide tension may be indicative of tissue hypoperfusion. Tatevossian and associates have demonstrated an increased mortality rate in patients with low oxygen or high carbon dioxide values (69). This technology is limited by the potential for thermal burns from the heated probes and tissue trauma from probe insertion (66).

Metabolic positron emission tomography Metabolic positron emission tomography (PET) is another noninvasive method for measuring oxygen transport and regional tissue oxygenation. With PET scanning, an isotope tracer is used to highlight blood flow and estimate oxygen delivery. Mintun and coworkers noted that oxygen levels in the brains of nine healthy volunteers had no correlation with blood flow (70). Regional oxygenation of the liver and myocardium have also been calculated (71, 72). The lack of transportability and cost of PET are the major deterrents to its implementation in the ICU setting.

Conclusions To prevent shock-related multiorgan failure, there is an urgent need to develop methods to accurately and rapidly recognize oxygen delivery and tissue hypoxia in the critically ill. Despite the large number of technologies available to clinicians, none individually is universally applicable or has been demonstrated to improve survival when resuscitative efforts are under way. Measurement of CaO2 and CO for the calculation of oxygen delivery is currently the most familiar approach for assessment of global DO2 . Regional assessments of tissue oxygenation, such as tissue goniometry, have yet to influence outcome. Newer methods, such as NIRS and OPS imaging, have allowed for continuous monitoring of oxygenation of individual organs. More research is necessary in the future to provide useful clinical

Chapter 10 – Oxygen Delivery, Oxygen Transport, and Tissue Oxygen Tension

devices for the quantification of adequency of regional tissue oxygenation in the critically ill.

References 1. Levy MM. Pathophysiology of oxygen delivery in respiratory failure. Chest 2005;128:547S–553S. 2. Greene KE, Peters JI. Pathophysiology of acute respiratory failure. Clin Chest Med 1994;15:1–12. 3. Leach RM, Treacher DF. Oxygen delivery and consumption in the critically ill. Thorax 2002;57:170–177. 4. Jolliet P, Thorens JB, Nicod L, et al. Relationship between pulmonary oxygen consumption, lung inflammation, and calculated venous admixture in patients with acute lung injury. Intensive Care Med 1996;22:277–285. 5. Marino PL. Oxygen and carbon dioxide transport. In The ICU Book, Third Edition. Philadelphia: Lippincott Williams & Wilkins, 2007, pp. 28–31. 6. Huang Y. Monitoring oxygen delivery in the critically ill. Chest 2005;128:554S–560S. 7. Schumacher PT, Cain SM. The concept of a critical DO2 . Intensive Care Med 1987;13:223. 8. Bihari D, Smithies M, Gimson A, et al. The effect of vasodilation with prostacyclin on oxygen delivery and uptake in critically ill patients. N Engl J Med 1987;317:397–403. 9. Velmahos GC, Demetriades D, Shoemaker WC, et al. Endpoints of resuscitation of critically injured patients: normal or supranormal? A prospective randomized trial. Ann Surg 2000;232(3):409–18. 10. Kern JW, Shoemaker WC. Meta-analysis of hemodynamic optimization in high-risk patients. Review. Crit Care Med 2002;30(8):1686–92. 11. Rivers EP, Coba V, Whitmaill M. Early goal-directed therapy in severe sepsis and septic shock: a contemporary review of the literature. Curr Opin Anaesthesiol 2008;21(3):424. 12. Rivers E, Nguyen B, Haystad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J Med 2001 Nov 8;345(19):1368–77. 13. Abou-Khalil B, Scalea TM, Trooskin SZ, et al. Hemodynamic responses to shock in young trauma patients: need for invasive monitoring. Crit Care Med 1994;22:633–9. 14. De Backer D, Creteur J, Dubois MJ, et al. The effect of dobutamine on microcirculation alterations in patients with septic shock are are independent of systemic effects. Crit Care Med 2006;34:403–8. 15. Peretz DI, Scott HM, Duff J, et al. The significance of lactic academia in the shock syndrome. Ann NY Acad Sci 1965;119:1133–41. 16. Vincent J-L, Dufaye P, Berre J, et al. Serial lactate determinations during circulatory shock. Crit Care Med 1983;11:449–51. 17. Falk JL, Rackow EC, Leavy J, et al. Delayed lactate clearance in patients surviving circulatory shock. Acute Care 1985;11: 212–5. 18. Abramson D, Scalea TM, Hitchcock R, et al. Lactate clearance and survival following injury. J Trauma 1993;35:584–9. 19. McNeilis J, Marini A, Jurkiewicz A, et al. Prolonged lactate clearance is associated with increased mortality in the surgical intensive care unit. Am J Surg 2001;182:481–2. 20. Mizock BA, Falk JL. Lactic acidosis in critical illness. Crit Care Med 1992;20:80. 21. Iberti TJ, Leibowitz AB, Papadakos PJ, et al. Low sensitivity of the anion gap as a screen to detect hyperlactatemia in critically ill patients. Crit Care Med 1990 Mar;18(3):275–7.

22. Davis JW. The relationship of base deficit to lactate in porcine hemorrhagic shock and resuscitation. J Trauma 1994;36: 168–72. 23. Bannon MP, O’Neill CM, Martin M, et al. Central venous oxygen saturation, arterial base deficit, and lactate concentration in trauma patients. Am Surg 1995;61:738–45. 24. Husain FA, Martin MJ, Mullenix PS, et al. Serum lactate and base deficit as predictors of mortality and morbidity. Am J Surg 2003;185(5):485–91. 25. Schmelzer TM, Perron AD, Thomason MH, et al. A comparison of central venous and arterial base deficit as a predictor of survival in acute trauma. Am J Emerg Med 2008;26(2):119–23. 26. Paladino L, Sinert R, Wallace D, et al. The utility of base deficit and arterial lactate in differentiating major from minor injury in trauma patients with normal vital signs. Resuscitation 2008;77(3):363–8. 27. Brill SA, Stewart TR, Brundage SI, et al. Base deficit does not predict mortality when secondary to hyperchloremic acidosis. Shock 2002;17:459–62. 28. Englehart MS, Schreiber MA. Measurement of acid-base resuscitation endpoints: lactate, base deficit, bicarbonate or what? Curr Opin Crit Care 2006;12:569–74. 29. Miller MJ, Cook W, Mithoefer J. Limitations of the use of mixed venous pO2 as an indicator of tissue hypoxia. Clin Res 1979;27:401. 30. Marx G, Reinhart K. Venous oximetry. Curr Opin Crit Care 2006;12:263–68. 31. Polanco PM, Pinsky MR. Practical issues of hemodynamic monitoring at the bedside. Surg Clin North Am. 2006;86(6):1431–56. 32. Lee J, Wright F, Barber R, et al. Central venous oxygen saturation in shock: study in man. Anesthesiology 1972;36:472–478. 33. Reinhart K, Kuhn HJ, Hartog C, et al. Continuous central venous and pulmonary artery oxygen saturation monitoring in the critically ill. Intensive Care Med 2004;30:1572–8. 34. Yazigi A, Khoury CE, Jebara S, et al. Comparison of central venous to mixed venous oxygen saturation in patients with low cardiac index and filling pressures after coronary artery surgery. J Cardiothorac Vasc Anesth 2008;22:77–83. 35. Chawla LS, Zia H, Gutierrez G, et al. Lack of equivalence between central and mixed venous oxygen saturation. Chest 2004;126:1891–6. 36. Dueck MH, Klimek M, Appenrodt S, et al. Trends but not individual values of central venous oxygen saturation agree with mixed venous oxygen saturation during varying hemodynamic conditions. Anesthesiology 2005;13:249–57. 37. Tahvanainen J, Meretoja O, Nikki P. Can central venous blood replace mixed venous blood samples? Crit Care Med 1982;10:758–61. 38. Poeze M, Solberg BC, Greve JW, et al. Monitoring global volume-related hemodynamic or regional variables after initial resuscitation: what is a better predictor of outcome in critically ill septic patients? Crit Care Med 2005;33:2494–2500. 39. Salman M, Glantzounis GK, Yang W, et al. Measurement of critical lower limb tissue hypoxia by coupling chemical and optical techniques. Clin Sci 2005;108:159–65. 40. Crookes BA, Cohn SM, Buton EA, et al. Noninvasive muscle oxygenation to guide fluid resuscitation after traumatic shock. Surgery 2004;135:662–70. 41. McKinley BA, Marvin RG, Cocanour CS, et al. Tissue hemoglobin O2 saturation during resuscitation of traumatic shock monitored using near infrared spectroscopy. J Trauma 2000;48:637–42.

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42. Pareznik R, Knezevic R, Voga G, et al. Changes in muscle tissue oxygenation during stagnant ischemia in septic patients. Intensive Care Med 2006;32:87–92. 43. De Blasi RA, Palmisani S, Alampi D, et al. Microvascular dysfunction and skeletal muscle oxygenation assessed by phase modulation near-infrared spectroscopy in patients with septic shock. Intensive Care Med 2005;31:1661–1668. 44. Creteur J, Carollo T, Soldati G, et al. The prognostic value of muscle StO2 in septic patients. Intensive Care Med 2007;33:1549–56. 45. Mulier KE, Skarda DE, Taylor JH, et al. Near-infrared spectroscopy in patients with severe sepsis: correlation with invasive hemodynamic measurements. Surg Infect 2008;9(5):515–9. 46. Marik PE, Bankov A. Sublingual capnometry versus traditional markers of tissue oxygenation in critically ill patients. Crit Care Med 2003;31:818–22. 47. Fink MP. Tissue capnometry as a monitoring strategy for critically ill patients: just about ready for prime time. Chest 1998;114:667–70. 48. Weil MH, Nakagawa Y, Tang W, et al. Sublingual capnometry: a new noninvasive measurement for diagnosis and quantitation of severity of circulatory shock. Crit Care Med. 1999;27:1225–9. 49. Marik PE. Regional carbon dioxide monitoring to assess the adequency of tissue perfusion. Curr Opin Crit Care 2005;11:245–51. 50. Porter J. Splanchnic circulation in shock. Trauma 1996;12:205–18. 51. Chang MC, et al. Gastric tonometry supplements information provided by systemic indicators of oxygen transport. J Trauma 1994;37:488–94. 52. Ivatury RR, et al. A prospective randomized study of end points of resuscitation after major trauma:global oxygen transport indices versus organ-specific gastric mucosal pH. J Am Coll Surg 1996;183:145–54. 53. Marik PE, Mohedin M. The contrasting effects of dopamine and norepinephrine on systemic and splanchic oxygen utilization in hyperdynamic sepsis. JAMA 1994;272(17):1354–7. 54. Duranteau J, Sitbon P, Teboul JL. Effects of epinephrine, norepinephine, or the combination of norepinephrine and dobutamine on gastric mucosa in septic shock. Crit Care Med 1999;27:2166–77. 55. Bouachour G, Guiraud MP, Gouello JP, et al. Gastric intramucosal pH and intraluminal PCO2 during weaning from mechanical ventilation in COPD patients. Eur Respir J 1996;9:1868–73. 56. Hurtado FJ, Beron M, Olivera W, et al. Gastric intramucosal pH and intraluminal PCO2 during weaning from mechanical ventilation. Crit Care Med 2001;29:70–76.

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57. Jin X, Weil MH, Sun S, et al. Decreases in organ blood flows associated with increases in sublingual PCO2 during hemorrhagic shock. J Appl Physiol 1998;85:2360–64. 58. Pernat A, Weil MH, Tang W, et al. Effects of hyper- and hypoventilation on gastric and sublingual PCO2 . J Appl Physiol 1999;87:933–7. 59. Nakagawa Y, Weil MH, Tang W, et al. Sublingual capnometry for diagnosis and quantitation of circulatory shock. Am J Respir Crit Care Med 1998;157:1838–43. 60. Povoas HP, Weil MH, Tang W, et al. Comparisons between sublingual and gastric tonometry during hemorrhagic shock. Chest 2000;118:1127–32. 61. Weil MH, Nakagawa Y, Tang W, et al. Sublingual capnometry: a new noninvasive measurement for diagnosis and quantification of severity of circulatory shock. Crit Care Med 1999;27(7):1225–9. 62. Dantzker DR. The gastrointestinal tract: the canary of the body? JAMA 1993;270:1247–48. 63. Marik PE. Sublingual capnography: a clinical validation study. Chest 2001;120:923–7. 64. Rackow EC, O’Neil P, Astiz ME, Carpati CM. Sublingual capnometry and indexes of tissue perfusion in patients with circulatory failure. Chest 2001;120:1633–8. 65. Wilson M, Davis DP, Coimbra R. Diagnosis and monitoring of hemorrhagic shock during the initial resuscitation of multiple trauma patients: a review. J Emerg Med 2003;24(4):413–22. 66. Winters ME, McCurdy MT, Zilberstein J. Monitoring the critically ill emergency department patient. Emerg Med Clin North Am 2008;26:741–57. 67. De Backer D, Creteur J, Preiser JC et al. Microvascular blood flow is altered in patients with sepsis. Am J Respir Crit Care Med 2002;166:98–104. 68. Lima A, Bakker J. Noninvasive monitoring of peripheral perfusion. Intensive Care Med 2005;31:1316–26. 69. Tatevossian RG, Wo CC, Velmahos GC, et al. Transcutaneous oxygen and CO2 as early warning of tissue hypoxia and hemodynamic shock in critically ill emergency patients. Crit Care Med 2000;28:2248–53. 70. Mintun MA, Lundstrom BN, Snyder AZ, et al. Blood flow and oxygen delivery to human brain during functional activity: theoretical modeling and experimental data. Proc Natl Acad Sci USA 2001;98:6859–64. 71. Piert M, Machulla HJ, Becker G, et al. Dependency of the 18F fluoromisonidazole uptake on the oxygen delivery and tissue oxygenation in the porcine liver. Nucl Med Biol 2000;27:693–700. 72. Porenta G, Cherry S, Czernin J, et al. Noninvasive determination of myocardial blood flow, oxygen consumption and efficiency in normal humans by carbon-11 acetate positron emission tomography imaging. Eur J Nucl Med 1999;26:1465–74.

Chapter

11

Transesophageal echocardiography Ronald A. Kahn and Gregory W. Fischer

Technical concepts Physics of ultrasound In ultrasonography, the heart and great vessels are insonated with ultrasound, which is sound above the human audible range. The ultrasound is sent into the area of interest and is partially reflected by the structures. From these reflections, distance, velocity, and density of objects are derived.

Wavelength, frequency, and velocity An ultrasound beam is a continuous or intermittent train of sound waves emitted by a transducer or wave generator. It is composed of density or pressure waves and can exist in any medium, with the exception of a vacuum. Ultrasound waves are characterized by their wavelength, frequency, and velocity. Wavelength is the distance between the two nearest points of equal pressure or density in an ultrasound beam, and velocity is the speed at which the waves propagate through a medium. As the waves travel past any fixed point in an ultrasound beam, the pressure cycles regularly and continuously between a high and a low value. The number of cycles per second (hertz) is called the frequency of the wave. Ultrasound is sound with frequencies above 20,000 Hz, which is the upper limit of the human audible range. The relationship among the frequency (f ), wavelength (␭), and velocity (v) of a sound wave is defined by the formula ␯ = f × ␭.

(11.1)

The velocity of sound varies with the properties of the medium through which it travels. For soft tissues, this velocity approximates 1540 m/sec. Because the frequency of an ultrasound beam is determined by the properties of the emitting transducer, and the velocity is a function of the tissues through which the sound travels, wavelengths vary according to the relationship expressed in Equation 11.1. Piezoelectric crystals convert between ultrasound and electrical signals. When presented with a high-frequency electrical signal, these crystals produced ultrasound energy, which is directed toward the areas to be imaged. Commonly, a short ultrasound signal is emitted from the piezoelectric crystal. After ultrasound wave formation, the crystal “listens” for the returning echoes for a given period of time and then pauses prior to

repeating this cycle. This cycle length is known as the pulse repetition frequency (PRF). This cycle length must be long enough to provide enough time for a signal to travel to and return from a given object of interest. Typically, PRFs vary from 1 to 10 kHz, which results in 0.1 to 1 msec between pulses. When reflected ultrasound waves return to these piezoelectric crystals, they are converted into electrical signals, which may be appropriately processed and displayed. Electronic circuits measure the time delay between the emitted and received echoes. Because the speed of ultrasound through tissue is a constant, this time delay may be converted into the precise distance between the transducer and tissue.

Attenuation, reflection, and scatter Waves interact with the medium in which they travel and with one another. Interaction among waves is called interference. The manner in which waves interact with a medium is determined by its density and homogeneity. When a wave is propagated through an inhomogeneous medium (and all living tissue is essentially inhomogeneous), it is partly reflected, partly absorbed, and partly scattered. Ultrasound waves are reflected when the width of the reflecting object is larger than one-fourth of the ultrasound wavelength. To visualize smaller objects, ultrasound waves of shorter wavelengths must be used. Because the velocity of sound in soft tissue is approximately constant, shorter wavelengths are obtained by increasing the frequency of the ultrasound beam. In addition, ultrasound impedance of the object must be significantly different from the ultrasonic impedance in front of the object. The ultrasound impedance of a given medium is equal to the medium density multiplied by the ultrasound propagation velocity. Air has a low density and propagation velocity, so it has a low ultrasound impedance. Bone has a high density and propagation velocity, so it has a high ultrasound impedance. Because the ultrasound impedances of air or bone are significantly different from that of blood, ultrasound is strongly reflected from these interfaces, limiting the availability of ultrasound to deeper structures. Echo studies across lung or other gas-containing tissues are not feasible, nor are those across bone. Reflected echoes, also called specular echoes, are usually much stronger than scattered echoes. A grossly inhomogeneous medium, such as a stone in a water bucket or a cardiac valve in

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a blood-filled heart chamber, produces strong specular reflections at the water–stone or blood–valve interface because of the significant differences in ultrasound impedances. Conversely, media that are inhomogeneous at the microscopic level, such as muscle, produce more scatter than specular reflection, because the differences in adjacent ultrasound impedances are low and the objects are small. Although smaller objects can be visualized with higher frequencies, more scatter is produced by insignificant inhomogeneities in the medium, confusing signals are generated, ultrasound beams are attenuated, and the depth of ultrasound penetration is limited. Attenuation refers to the loss of ultrasound power as it traverses tissue. Tissue attenuation is dependent on ultrasound reflection, scattering, and absorption. The absorption occurs as a result of the conversion of ultrasound energy into heat. The greater the ultrasound reflection and scattering, the less ultrasound energy is available for penetration and resolution of deeper structures; this effect is especially important during scanning with higher frequencies. Whereas water, blood, and muscle have low ultrasound attenuation, air and bone have very high tissue ultrasound attenuation, limiting the ability of ultrasound to traverse these structures.

Image formation M mode The most basic form of ultrasound imaging is M-mode echocardiography. In this mode, the density and position of all tissues in the path of a narrow ultrasound beam (i.e. along a single line) are displayed as a scroll on a video screen. The scrolling produces an updated, continuously changing time plot of the studied tissue section, several seconds in duration. Because this is a timed motion display (normal cardiac tissue is always in motion), it is called M mode. Because only a very limited part of the heart is being observed at any one time and because the image requires considerable interpretation, M mode is not currently used as a primary imaging technique.

2D mode By rapid, repetitive scanning along many different radii within an area in the shape of a fan (sector), echocardiography generates a two-dimensional (2D) image of a section of the heart. This image, which resembles an anatomic section and, thus, can be more easily interpreted, is called a 2D scan. Information on structures and motion in the plane of a 2D scan is updated 30 to 60 times per second. This repetitive update produces a live (realtime) image of the heart. Scanning 2D echo devices image the heart by using either a mechanically steered transducer or, as is common in most devices, an electronically steered ultrasound beam (phased-array transducer).

Doppler techniques Most modern ultrasound scanners combine Doppler capabilities with their 2D imaging capabilities. After the desired view

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has been obtained by 2D ultrasonography, the Doppler beam, represented by a cursor, is superimposed on the 2D image. The operator positions the cursor as parallel as possible to the assumed direction of blood flow and then empirically adjusts the direction of the beam to optimize the audio and visual representations of the reflected Doppler signal. At the present time, Doppler technology can be used in at least four different ways to measure blood velocities: pulsed, continuous-wave, and color-flow.

The Doppler effect Information on blood flow dynamics can be obtained by applying Doppler frequency shift analysis to echoes reflected by the moving red blood cells. Blood flow velocity, direction, and acceleration can be instantaneously determined. This information is different from that obtained in 2D imaging and hence complements it. The Doppler principle, as applied in echocardiography, states that the frequency of ultrasound reflected by a moving target (red blood cells) will be different from the frequency of the reflected ultrasound. The magnitude and direction of the frequency shift are related to the velocity and direction of the moving target. The velocity of the target is calculated with the Doppler equation: v = (c f d )/(2 f 0 cos ␪),

(11.2)

where v = the target velocity (blood flow velocity), c = the speed of sound in tissue, fd = the frequency shift, f0 = the frequency of the emitted ultrasound, and ␪ = the angle between the ultrasound beam and the direction of the target velocity (blood flow). The only ambiguity in Equation 11.2 is that, theoretically, the direction of the ultrasonic signal could refer to either the transmitted or the received beam; however, by convention, Doppler displays are made with reference to the received beam. Thus, if the blood flow and the reflected beam travel in the same direction, the angle of incidence is zero degrees and the cosine is +1. As a result, the frequency of the reflected signal will be higher than the frequency of the emitted signal. Equipment currently used in clinical practice displays Doppler blood flow velocities as waveforms. The waveforms consist of a spectral analysis of velocities on the ordinate and time on the abscissa. By convention, blood flow toward the transducer is represented above the baseline. If the blood flows away from the transducer, the angle of incidence will be 180 degrees, the cosine will equal –1, and the waveform will be displayed below the baseline. When the blood flow is perpendicular to the ultrasonic beam, the angle of incidence will be 90 or 270 degrees, the cosine of either angle will be zero, and no blood flow will be detected. Because the cosine of the angle of incidence is a variable in the Doppler equation, blood flow velocity is measured most accurately when the ultrasound beam is parallel or antiparallel to the direction of blood flow. In clinical practice, a deviation from parallel of up to 20 degrees can

Chapter 11 – Transesophageal Echocardiography

be tolerated, because this results in an error of only 6 percent or less.

Pulsed-wave Doppler In pulsed-wave (PW) Doppler, blood flow parameters can be determined at precise locations within the heart by emitting repetitive short bursts of ultrasound at a specific frequency (the PRF) and analyzing the frequency shift of the reflected echoes at an identical sampling frequency (fs ). A time delay between the emission of the ultrasound signal burst and the sampling of the reflected signal determines the depth at which the velocities are sampled. The delay is proportional to the distance between the transducer and the location of the velocity measurements. To sample at a given depth (D), sufficient time must be allowed for the signal to travel a distance of 2 × D (from the transducer to the sample volume and back). The time delay, Td , between the emission of the signal and the reception of the reflected signal is related to D and to the speed of sound in tissues (c) by the following formula: D = c Td /2.

(11.3)

The operator varies the depth of sampling by varying the time delay between the emission of the ultrasonic signal and the sampling of the reflected wave. In practice, the sampling location or sample volume is represented by a small marker, which can be positioned at any point along the Doppler beam by moving it up or down the Doppler cursor. On some devices, it is also possible to vary the width and height of the sample volume. The tradeoff for the ability to measure flow at precise locations is that ambiguous information is obtained when flow velocity is very high. A simple reference to Western movies will clearly illustrate this point. When a stagecoach gets under way, its wheel spokes are observed as rotating in the correct direction. As soon as a certain speed is attained, rotation in the reverse direction is noted because the camera frame rate is too slow to correctly observe the motion of the wheel spokes. In PW Doppler, the ambiguity exists because the measured Doppler frequency shift (fD ) and the sampling frequency (fs ) are in the same frequency (kilohertz) range. Ambiguity will be avoided only if the fD is less than half the sampling frequency. The expression fs /2 is also known as the Nyquist limit. Doppler shifts above the Nyquist limit will create artifacts described as “aliasing” or “wraparound,” and blood flow velocities will appear in a direction opposite to the conventional one. Blood flowing with high velocity toward the transducer will result in a display of velocities above and below the baseline. This artifact can be avoided by increasing the fs , but this then limits the time available for a pulse to travel to the sample volume and back, thus limiting the range.

Continuous-wave Doppler The continuous-wave (CW) Doppler technique uses continuous, rather than discrete, pulses of ultrasound waves. As a result, the region in which flow dynamics are measured cannot be

precisely localized. Blood flow velocity is measured with great accuracy, however, even at high flows. CW Doppler is particularly useful for the evaluation of patients with valvular lesions or congenital heart disease. It is also the preferred technique when attempting to derive hemodynamic information from Doppler signals.

Color-flow mapping During color-flow Doppler (CFD) mapping, real-time blood flow within the heart as colors, along with 2D images in black and white, are displayed. In addition to showing the location, direction, and velocity of cardiac blood flow, the images produced by these devices allow estimation of flow acceleration and differentiation of laminar and turbulent blood flow. CFD echocardiography is based on the principle of multigated PW Doppler, in which blood flow velocities are sampled at many locations along many lines covering the entire imaging sector. At the same time, the sector is also scanned to generate a 2D image. A location in the heart in which the scanner has detected flow toward the transducer (the top of the image sector) is assigned the color red. Flow away from the direction of the top is assigned the color blue. This color assignment is arbitrary and determined by the equipment’s manufacturer and the user’s color mapping. In the most common color-flow coding scheme, the faster the velocity, the more intense the color. Flow velocities that change by more than a preset value within a brief time interval (flow variance) have another color added to either the red or the blue. Both rapidly accelerating laminar flow (change in flow speed) and turbulent flow (change in flow direction) satisfy the criteria for rapid changes in velocity. In summary, the brightness of the red or blue colors at any location and time is usually proportional to the corresponding flow velocity, and the hue is proportional to the temporal rate of change of the velocity.

Technical concepts of 3D echocardiography Two different technological approaches are available for acquiring three-dimensional (3D) images. The first technique requires the acquisition of multiple, gated image planes using ECG and respiratory gating to limit the amount of motion artifacts. Once a region of interest is identified, the probe rotates from zero to 180 degrees acquiring different 2D images every few degrees. After all 2D images are acquired and stored, they are postprocessed and integrated into a 3D image that can further be optimized. Real-time, instantaneous imaging can never be obtained using this technology because of the sequential acquisition of the different planes. Additionally, the gating requirements of this technology (e.g. 90 or more 2D planes) frequently result in motion artifacts. The gated technique uses the same technology that is currently employed for standard 2D scanning. One-dimensional arrays, consisting of 128 piezoelectric crystals that are interconnected electronically, generate an acoustic beam that can be steered in a flat scanning plane (axial and

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Figure 11.2. Live 3D real-time scanning showing a 3D volume pyramid. (See Color Plate II.)

Display of 3D images Figure 11.1. Matrix array with 2500 independent elements representing the basis for real-time 3D scanning. Human hair is shown to better demonstrate dimensions. (See Color Plate I.)

lateral planes). This to-and-fro sweeping motion of the acoustic beam across the sector represents the basis of any phased array transducer system. This technology is available for both transthoracic and transesophageal acquisition and is supported by multiple platforms. The second technology is based on a matrix array design of the piezoelectric crystals within the transducer head, allowing for real-time volumetric scanning (Figure 11.1). The matrix array, as opposed to the standard 1D array, is a 2D array, consisting of 50 rows and 50 columns of elements. Whereas in a 1D array only 128 elements need to be controlled independently of one another, the matrix technology requires independence of the 2500 elements all in the confined space of the head of a sonographic probe. This 2D array enables the generation of scan line that can be steered not only in the axial and lateral dimensions, but also in the elevational dimension. Even though one would expect that imaging the heart in three dimensions should result in better understanding of the topographical anatomy of different intracardiac structures and how they interact with one another during the cardiac cycle, it must be emphasized that the same constraints of 1D and 2D echocardiography apply for 3D echocardiography. Sector size, resolution, and frame rate interact with one another. Increasing the requirements of one will lead to deterioration in either or both. Three-dimensional echocardiography is subject to the same laws of acoustic physics as 2D echocardiography. Artifacts such as ringing, reverberations, shadowing, and attenuation occur in 3D as well as in 2D and M-mode. Two platforms currently support this technology for transthoracic scanning; however, only one has a fully functional real-time 3D transesophageal echocardiography (TEE) probe.

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Classical views acquired in 2D echocardiography are not required in 3D echocardiography, because entire volumetric datasets are acquired that can be spatially oriented at the discretion of the echocardiographer. The electronically steered 3D TEE has two modes of operation. The first is a live mode in which the system scans in real-time 3D. The second integrates only four to eight gated beats (as opposed to ⬎90), which enables wider volumes to be generated while maintaining frame rate and resolution.

Live 3D – real time In this mode, a 3D volume pyramid is obtained. The image shown in this mode is in real time. The 3D image changes as the transducer is moved, just as in the live 2D imaging case. Manipulations of the TEE probe (e.g. rotation, change in position) lead to instantaneous changes in the image seen on the monitor (Figure 11.2).

3D zoom – real time Besides the superior acquisition of ventricular volumes and function, the main advantage of the 3D TEE compared with conventional 2D transducers lies in its ability to obtain realtime images of the mitral valve (MV) apparatus. The best way to image the MV live is with the 3D zoom mode. This mode displays a small magnified pyramidal volume of the MV which may vary from 20◦ × 20◦ up to 90◦ × 90◦ , depending on the density setting. This small dataset can be spatially oriented at the discretion of the echocardiographer, enabling views of the MV from both the left atrium (LA) and left ventricle (LV) perspectives. The real-time (RT) 3D images are devoid of rotational artifacts, as are commonly encountered with ECG gated 3D acquisitions (Figure 11.3).

Full volume – gated Three-dimensional imaging is limited not by computer and circuit processing power, but simply by the speed of sound. There is insufficient time for sound to travel back and forth in large

Chapter 11 – Transesophageal Echocardiography

Figure 11.3. 3D zoom mode. En face view of mitral valve after repair and annuloplasy. This view is real-time and devoid of ECG artifacts. (See Color Plate III.)

Figure 11.5. Same image as shown in Figure 11.4. The operator has spatially reoriented the dataset and started to crop with the intent to better expose a region of interest. (See Color Plate V.)

volumes while maintaining a frame rate of ⬎20 Hz and reasonable resolution in live scanning modes. One maneuver to overcome this limitation entails stitching four to eight gates together to create a full-volume mode. These gated slabs or subvolumes represent a pyramidal 3D dataset, as would be acquired in the live 3D mode. This technique can generate ⬎90-degree scanning volumes at frame rates greater than 30Hz. Increasing the gates from four to eight creates smaller 3D slabs; this can be used to maintain frame rates and/or resolution as the volumes (pyramids) become larger (Figure 11.4). Gating refers to the ability to analyze ECG RR intervals, discarding errant subvolumes if the intervals are too irregular. As with any conventional gating techniques, patients with arrhythmias are prone to motion artifacts when the individual datasets are combined. As long as the RR intervals fall within a reasonable range, a full-volume dataset can still be reconstructed (e.g. atrial fibrillation, electrocautery artifact). The acquired RT 3D dataset can subsequently be cropped, analyzed, and quantified using integrated software in the 3D operating system (QLAB; Philips Healthcare, Andover, MA) (Figures 11.5 and 11.6).

frequency shifts among these transmited pulses. Structures that do not move maintain the same Doppler frequency spectrum. Unfortunately, firing more events along a stationary scan line deteriorates the frame rate. To increase the frame rate, a gating method must be used, similar to that of the fullvolume mode; however, because of the large amount of data required, eight to eleven beats are needed to be combined to create an image. Jet direction, extent, and geometry can easily be recognized using this technique. Reports started emerging a decade ago showing that the strength of this methodology lies in its ability to quantify the severity of regurgitant lesions. Three-dimensional quantification of mitral regurgitation correlates better than 2D imaging, when using angiography as the gold standard.1 In an experimental setting, 3D quantification was more accurate (2.6% underestimation) than 2D or M-mode methods, which had the tendency to underestimate regurgitant volumes (44.2% and 32.1%, respectively)2 (Figure 11.7).

3D color Doppler – gated CFD requires obtaining multiple samples along a common scan line. Tissue or blood velocity is determined by analyzing

Figure 11.4. Full volume image. Four to eight ECG gated slabs are stitched together, enabling the acquisition of a larger volume without loss of frame rate or resolution. (See Color Plate IV.)

Figure 11.6. The 3D dataset can be quantified using semiautomatic software. The model created shows the relationship of the leaflet to the annular plane (red above, blue below). True volumes and unforeshortened distances can be measured. (See Color Plate VI.)

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Transgastric two chamber

Figure 11.7. 3D color Doppler gated. Concentric jet originating from P2. Valve viewed from anterior to posterior. (See Color Plate VII.)

Parameters monitored Twenty standard American Society of Echocardiography views Transgastric midpapillary short axis The probe is advanced into the stomach and slightly anteroflexed until the posterolateral and anterolateral papillary muscles are visualized at their attachment to the ventricular wall (Figure 11.8). It is important to image the insertion of the papillary muscles to ensure accurate intra- and interobserver examinations. The LV is centered on the screen. If the MV apparatus is visualized, the probe should be either further advanced or posteroflexed. Similarly, if the ventricular apex is visualized, the probe should be either withdrawn or anteroflexed. All six middle segments of the ventricle are visualized, which represents perfusion from each of the three coronary arteries. The size and function of both the right and left ventricle may be evaluated. Although qualitative evaluation of right ventricular function may be performed, quantitative measurement of left ventricular fractional area of shortening may be calculated. Regional wall motion abnormalities may be visualized, which may represent myocardial ischemia.

From the transgastric midpapillary short axis view with the ventricle centered in the screen, the array is rotated to 90◦ (Figure 11.9). The length of the LV should be optimized to avoid foreshadowing. The apical, middle, and basal segments of both the anterior and inferior walls of the LV may be evaluated. The anterior and posterior leaflets of the MV can be visualized. The base of anterolateral aspect of the anterior MV leaflet (A1) through the tip of posteriomedial aspect of the anterior leaflet (A3) may be visualized, as it coapts with the posteriomedial scallop of the posterior leaflet (P3). The subvalvular MV apparatus may be evaluated even in the presence of heavy mitral valvular calcification. The left atrial appendage can be evaluated for thrombus.

Transgastric long axis As the array is rotated to approximately 120◦ , the long axis of the left ventricular outflow is visualized (Figure 11.10). The angle of the array should be optimized to included the left ventricular apex, the left ventricular outflow tract, aortic valve, and the proximal aspect of the ascending aorta. The apical, middle, and basal aspects of the anteroseptal and inferolateral (posterior) left ventricular walls can be seen. The direction of left ventricular outflow through the aortic valve may be parallel to the ultrasonic beam, to allow for calculation of gradient across the aortic valve and calculation of aortic valve area. CFD may be used to evaluate the severity of aortic regurgitation.

Transgastric right ventricular inflow From the transgastric long axis view, the probe is rotated right to visualize the right atrium and ventricle (Figure 11.11). The anterior and posterior leaflets of the tricuspid valve may be seen. Right ventricular size and function can be evaluated, as well as the severity of the tricuspid regurgitation.

Deep transgastric long axis The array is rotated back to 0◦ and is advanced further into the stomach to the ventricular apex (Figure 11.12). The probe is

Figure 11.8. Transgastric midpapillary short axis. RV = right ventricle, LV = left ventricle.

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Figure 11.9. Transgastric two chamber. LA = left atrium, RV = right ventricle, LV = left ventricle.

Figure 11.10. Transgastric long axis. LA = left atrium, LV = left ventricle, LAA = left atrial appendage.

Figure 11.11. Transgastric right ventricular inflow. RA = right atrium, LA= left atrium.

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Figure 11.12. Deep transgastric long axis. LA = left atrium, RV = right ventricle, LV = left ventricle, AV= aortic valve.

severely anteroflexed and directed toward the ventricular base. As in the transgastric long axis view, the anteroseptal and inferolateral wall may be visualized. The axis of left ventricular outflow is usually optimized with the direction of the ultrasonic beam, allowing for accurate estimations of both aortic stenosis and regurgitation. The subvalvular apparatus of the mitral valve may be evaluated for severity of calcification.

Transgastic basal short axis As the probe is withdrawn from the deep transgastric long axis view, though the transgastric midpapillary view, the transgastric basal short axis view may be obtained (Figure 11.13). The basal aspects of the walls of the LV may be visualized. Both the anterior and posterior MV leaflet tips are seen, allowing for visualization of the MV leaflet tips. Restriction of leaflet opening may be visualized and localized if mitral stenosis is present. If CFD is used, spatial localization of MV regurgitation may be identified within the opening of the MV; however, localization of

Figure 11.13. Transgastric basal short axis. LV = left ventricle.

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pathology to the anterior or posterior leaflet is usually not possible with this view.

Midesophageal four chamber Maintaining the probe at approximately 0◦ , the probe is withdrawn into the mid-esophagus (Figure 11.14). Slight anteroflexion is usually necessary to avoid foreshortening of the LV. The array may need to be rotated approximately 10◦ to avoid imaging the left ventricular outflow tract and optimize visualization of the basal aspect of the inferoseptal left ventricular wall. In this view, the basal, middle, and apical aspects of the anterolateral and inferoseptal LV walls may be evaluated. Left and right atrial sizes may be evaluated by measuring atrial diameter; left atrial size may be further described by the measurement of the distance between the MV annular plane and the left atrial dome. The presence of left atrial spontaneous echo contrast (“smoke”) may be observed in patients with left atrial stasis, and the left atrial appendage may be examined for evidence of thrombus.

Chapter 11 – Transesophageal Echocardiography

Figure 11.14. Midesophageal four chamber. LA = left atrium, RA = right atrium, LV = left ventricle, RV = right ventricle.

Right ventricular size and function may evaluated. Whereas estimation of right ventricular ejection fraction is limited by the complex geometric shape of the right ventricle, changes in the distance between the tricuspid annulus and the right ventricular apex may be used as a measurement of right ventricular function. Both anterior and posterior leaflets of the MV may be imaged and evaluated for motion and pathology. With the echo probe optimally retroflexed with full visualization of the left ventricular apex, the most posteriomedial aspects of the anterior and posterior MV leaflets are usually imaged. As the probe is either slowly anteroflexed or withdrawn, the middle and, finally, anterolateral apects of these leaflets may be imaged. The septal and posterior tricuspid valve leaflets are usually visualized; however, if the probe is withdrawn too far or is too far anteroflexed, the anterior tricuspid valve leaflet may be visualized instead of the posterior leaflet. Pulse wave Doppler at the level of the MV leaflet tips may be used to evaluate diastolic

function and the severity of mitral stenosis. With moderate to severe mitral stenosis, continuous wave Doppler will probably need to be employed. Tissue Doppler measurements of the MV annulus, as well as color M-mode imaging of left ventricular inflow, may be used to evaluate left ventricular diastolic function. CFD may be used to evaluate the severity of mitral and tricuspid regurgitation as well as the presence of an atrial septal defect. Because of the low expected gradients between the atria, a low CFD setting will need to be employed to appreciate interatrial flow if it is present.

Midesophageal mitral commissural The posterior leaflet is shaped like a crescent, whereas the anterior leaflet has an oblong shape as it coapts within this crescent (Figure 11.15). In the commissural view, the MV is imaged across this commissural opening with the anterolateral (P1) and posteromedial (P3) scallops of the posterior leaflet at either side of the image, with the middle aspect of the anterior leaflet (A2)

Figure 11.15. Midesophageal mitral commissural. LA = left atrium, LV = left ventricle, LCxA = left circumflex artery.

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Figure 11.16. Midesophageal two chamber. LA = left atrium, LV = left ventricle, LAA = left atrial appendage.

in the middle of the MV opening. With the MV centered in the image and the apex of the LV imaged, the array is rotated to approximately 60◦ , so both the posteromedial scallop of the posterior leaflet (P3) and P1 are visualized. A2 will be seen between these two leaflet scallops. This view provides a high degree of confidence that both P1 and P3 are being imaged accurately. P3 restriction may be observed with ischemic mitral regurgitation. The MV commissural opening may be visualized, and the motion of these leaflet segments may be evaluated. Color Doppler is helpful in the localization of the site of MV regurgitation (i.e. anterolateral versus posteromedial commissure) as well as the severity of mitral regurgitation.

Midesophageal two-chamber Further rotation of the transducer array to 90◦ will develop the midesophageal two-chamber view (Figure 11.16). Similar to the transgastric view, all segments of the anterior and inferior left ventricular walls may be evaluated for thickness and contractility. The anterior and posterior leaflets of the MV are imaged,

and evidence of stenosis and regurgitation may be obtained. The left atrial size may be measured and smoke may be imaged if present. The left atrial appendage can be examined for thrombus, which is not uncommon with left atrial stasis. Withdrawal of the probe will allow for imaging of both the upper and lower pulmonary veins; their Doppler evaluation will allow qualitative estimates of left atrial pressure and severity of mitral regurgitation.

Midesophageal long axis Similar to the midesophageal two-chamber view, this midesophageal view of the left ventricular long axis usually provides better resolution than its transgastric equivalent (Figure 11.17). Further rotation to 120◦ develops the long axis view. A single axis from the left ventricular apex to the left ventricular outflow tract to the aortic valve to the ascending aorta should be developed. Further rotation to 130◦ or 140◦ may be necessary to obtain this axis alignment with cardiac rotation. In this view, both segments (basal and middle) of the anteroseptal and

Figure 11.17. Midesophageal long axis. LA = left atrium, RV = right ventricle, LV = left ventricle, Ao= aorta.

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Figure 11.18. Midesophageal aortic valve short axis. LA = left atrium, RA = right atrium, PA = pulmonary artery, NC = noncoronary cusp, RC = right coronary cusp, LC = left coronary cusp.

inferolateral walls may be seen and evaluated. The A2 and P2 segments of the mitral valve may be seen and evaluated for motion. P2 restriction may be seen with ischemic cardiac disease, and systolic anterior motion of the anterior MV leaflet may be easily appreciated with hypertrophic obstructive cardiomyopathy in this view. The severity of mitral regurgitation may be estimated by CFD.

be attempted in this view; however, its use may be limited by shadowing caused by valvular calcification. CFD may be used to identify the site of aortic valve regurgitation, but quantification using this view may be difficult. The left main coronary artery may be imaged as it emerges adjacent to the left coronary cusp. Its bifurcation into the left anterior descending and circumflex artery is occasionally appreciated.

Midesophageal aortic valve short axis

Midesophageal aortic valve long axis

Attention is now directed toward the aortic valve (Figure 11.18). The aortic valve is centered on the screen and the array is rotated to approximately 30◦ . The three cusps of the aortic valve (right, left, and noncoronary) may be visualized, along with its triangular opening. Evidence of pathology on the aortic valve cusps may be appreciated. Aortic valve stenosis may be estimated qualitatively by observing the aortic valve leaflet opening. Quantization of aortic stenosis by planimetry may

The transducer array is rotated to 120◦ to develop the midesophageal aortic valve long axis view (Figure 11.19). The orientation of the image is similar to that of the midesophageal long axis. The right coronary cusp of the aortic valve may be visualized anteriorly; the posterior cusp is either the right or the noncoronary cusp. Rightward (clockwise) rotation of the probe will favor visualization of the right coronary cusp, whereas leftward (counterclockwise) rotation will favor visualization of the

Figure 11.19. Midesophageal aortic valve long axis. LA = left atrium, RV = right ventricle, LV = left ventricle, AV = aortic valve.

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Figure 11.20. Midesophageal ascending aortic long axis. PA = pulmonary artery.

noncoronary cusp. The diameters of the aortic valve annulus, sinus of Valsalva, and the sinotubular junction may be measured. The severity of aortic regurgitation may be evaluated by examining the size of the aortic regurgitant jet as it extends into the left ventricular outflow tract. The right coronary artery can be visualized as it exits the aorta anteriorly. Proximal ascending aortic pathology may be evaluated.

Midesophageal ascending aortic long axis The probe is further withdrawn to visualize the ascending aorta (Figure 11.20). Because of the interposition of the esophagus and either the trachea or bronchus, the distal ascending aorta usually cannot be visualized. The proximal and middle sections of the aorta can usually be seen and examined for atherosclerotic disease up to the crossing of the right pulmonary artery. More detailed examination of the ascending aorta at potential aortic cannulation and cross-clamp sites for cardiac surgery

require epiaortic imaging, which is a sensitive modality for the detection of atherosclerotic disease.

Midesophageal right ventricular inflow–outflow The transducer array is returned to 0◦ and the four-chamber view is redeveloped (Figure 11.21). The tricuspid valve is centered on the screen and the array is rotated to approximately 60◦ . In addition to the left atrium, the right atrium, tricuspid valve, right ventricle, right ventricular outflow tract, pulmonary valve, and proximal pulmonary artery may be visualized. The septal and anterior leaflets of the tricuspid valve may be seen. CFD may be superimposed, evaluating the severity of tricuspid regurgitation. Moving the color Doppler field to the pulmonary valve allows estimation of pulmonary regurgitation. If there is tricuspid regurgitation, continuous-wave Doppler may be used to estimate systolic pulmonary artery pressure.

Figure 11.21. Midesophageal right ventricular inflow–outflow. LA = left atrium, RA = right atrium, RV = right ventricle, RVOT = right ventricular outflow tract, AV = aortic valve, PA = pulmonary artery.

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Figure 11.22. Midesophageal bi-caval. LA = left atrium, RA = right atrium, SVC = superior vena cava, IVC = inferior vena cava.

Midesophageal bi-caval If the array is rotated to approximately 90◦ and rotated clockwise, the bi-caval view may be obtained (Figure 11.22). The superior and inferior vena cava may be visualized as they enter the right atrium. The eustachian valve may be seen as a fibrinous structure at the junction of the inferior vena cava with the right atrium. Septum secundum may be visualized as it extends from the inferior aspect of the right atrium superiorly, and the septum primum may be visualized as it extends from the superior aspect of the right atrium. Low-velocity CFD may be used to visualize atrial septal defects, which are usually leftto-right flows. The intravenous injection of contrast (such as agitated saline) with the release of Valsalva may reveal rightto-left flow through a patent foramen ovale. Further rightward rotation allows visualization of the right upper and lower pulmonary veins as they enter the left atrium.

Midesophageal ascending aortic short axis The array probe is returned to 0◦ and the aortic valve is once again centered on the screen (Figure 11.23). The probe is

withdrawn through the base of the heart until the pulmonary artery and its bifurcation are imaged. The severity of proximal and middle ascending aortic atherosclerosis and pathology may be evaluated. If a clear view of the ascending pulmonary artery is obtained, Doppler imaging may be used to estimate stroke volume.

Descending aortic short axis and upper esophageal aortic arch long axis The probe is turned leftward toward the descending thoracic aorta. Because the probe is severely rotated, the orientation of the images will have changed. The top of the image is now the anteromedial aortic wall, and the bottom of the image is the posterolateral wall. The probe is advanced toward the stomach until the image is lost. The probe is withdrawn slowly, thus imaging the entire descending aorta. The presence of atherosclerotic disease should be noted. The probe is withdrawn until the level of the upper esophagus, where a long axis view of the aortic arch may be seen.

Figure 11.23. Midesophageal ascending aortic short-axis. SVC = superior vena cava, PA = pulmonary artery.

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Descending aortic long axis and upper esophageal aortic arch short axis

important not to confuse FS with fractional area change or ejection fraction.

The probe is returned to the stomach and the array is rotated to 90◦ to develop a long axis view of the descending aorta. Once again, the probe is withdrawn slowly. It may be necessary to rotate the probe right and left to optimize this long axis visualization. The arch is visualized in the upper esophageal area when a cross-sectional image is developed. At this point, the probe generally does not need to be withdrawn further. The probe is rotated anteriorly, allowing for visualization of the left subclavian, left carotid, and right innominate arteries as they exit the aortic arch. The left and main pulmonary arteries may be visualized. The left innominate vein may be seen anteriorly and superiorly to the aortic arch, which may be misdiagnosed as an aortic dissection.

Left ventricular wall thickness

Derived information Evaluation of right and left ventricular size and function The ability to assess ventricular function noninvasively is one of the most commonly posed questions to the echocardiographer. Assessment of ventricular function is unfortunately not as straightforward as one might think. The ideal measurement would be simply obtainable, reproducible, and independent of loading conditions placed on the ventricle. As surrogates, echocardiographers use a vast array of measurements.

One-dimensional measurements (linear) M-mode has the advantage of high frame rates, leading to exceptional temporal resolution. A disadvantage to this method is the fact that the ventricle is being interrogated solely along a single line (ice pick). Although geometric assumptions can be made that correlate well with normal ventricular size and function, limitations are quickly reached once regional wall motion abnormalities or deviations from normal ventricular size appear.

Fractional shortening A common measurement representing LV function is fractional shortening (FS). This measurement is derived by measuring the LV internal diameter in diastole and subtracting it from the LV internal diameter (LVID) measured in systole: ((LVIDd − LVIDs)/LVIDd) × 100. A transgastric two-chamber view is ideal for obtaining this measurement. LV diameters are measured from the endocardium of the inferior wall to the endocardium of the anterior wall in a line perpendicular to the long axis of the ventricle at the junction of the basal and middle segments of the anterior and inferior walls. Normal values are 25 percent to 43 percent in men and 27 percent to 45 percent in women.3 It is

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Left ventricular wall thickness is measured to diagnose ventricular hypertrophy. Normal values are less than 10 mm for men and less than 9 mm for women.3 The TG midpapillary short axis view is acquired at end-diastole and the thickness of the septum and posterior wall measured.

Derived from these two measurements: relative wall thickness The relative wall thickness (RWT) is used to subdivide the different forms of ventricular hypertrophy (eccentric vs. concentric): RWT = (PWTd + SWTd)/LVIDd. RWT ⬎ 0.42 is indicative for concentric hypertrophy, whereas RWT ⬍ 0.42 is typically found in eccentric hypertrophy.

Left ventricular mass Left ventricular mass is the parameter most commonly used to evaluate the success of treatment trials in epidemiologic studies.4 Mass is derived by subtracting left ventricular cavity volume from the volume of the LV in its entirety. This shell volume is then converted to mass by multiplying by myocardial density. The American Society of Echocardiography (ASE) recommends the use of the following formula to calculate LV mass: LVmass = 0.8 × (1.04[(LVIDd + PWTd + SWTd)3 −(LVIDd)3 ]) + 0.6g, where LVIDd = left ventricular internal diastolic diameter in diastole, PWT = posterior wall thickness, and SWT = septal wall thickness.3 This formula was found to have a high level of correlation with LV mass found at autopsies (r = 0.9, p = 0.001).5

Two-dimensional assessment of ventricular function Fractional area change The fractional area change (FAC) is the parameter most often requested from the echocardiographer. Although this measurement is dependent on loading conditions, it is frequently used to guide clinical management of patients with cardiovascular disease. This measurement is conceptionally simple and reproducible. The LV cavity is imaged in a transgastric midpapillary SAX view, and the area measured in end-systole and enddiastole. The difference divided by the area in end-diastole represents the FAC: FAC (%) = [(LVAd − LVAs)/LVAd] × 100

Chapter 11 – Transesophageal Echocardiography

Normal values are 56 percent to 63 percent in men and 59 percent to 65 percent in women.3 The FAC should not be confused with the ejection fraction (EF) or fractional shortening. The FAC is a change in area, whereas the EF is a change in volume and fractional shortening is a change in length. In normal hearts there is a good correlation between the FAC and EF; however, in the setting of abnormal ventricular geometry (e.g. aneurysm), the relationship no longer applies.

3D assessment of LV function Geometric assumptions applied to the LV allow estimation of volumetric measurements based on 2D measurements. The most commonly used formula is the biplane method of disks or Simpson’s modified rule. The LV volume is calculated by summing a stack of elliptical disks that are superimposed along the long axis of the LV. Two views that are orthogonal to each other are recommended; most commonly, the four-chamber and twochamber views are used for this purpose (Figure 11.24). Unfortunately, there are multiple shortcomings when volumes are calculated based on these geometric assumptions. First, the LV must be elliptical in shape. This is true only for normal ventricles. Patients who have impaired ventricular function (where EF is of great interest) are the ones with altered geometry. Second, the placement of the 2D plane can be subject to positioning errors, which may lead to chamber foreshortening. Although these errors were accepted in the past as unavoidable, the emergence of 3D imaging will most likely change the playing field, as 3D echocardiography does not rely on geometric assumptions for volume and/or mass calculations. Studies comparing LV volumes and mass measured by 3D echocardiography, 2D echocardiography, and magnetic resonance imaging (MRI), which is the gold standard, showed significantly better

Figure 11.24. Transgastric short axis view of left ventricle. Large pericardial effusion seen surrounding the LV.

Figure 11.25. Semiautomatic software with endocardial border detection capability enabling the measurement of true ventricular volumes and calculation of a true ejection fraction. (See Color Plate VIII.)

correlation between 3D echocardiography and MRI than between 2D echocardiography and MRI (Figure 11.25).6–8

Right ventricle The right ventricle (RV) is a complex crescent-shaped structure that does not lend itself as easily to geometric assumptions as its left ventricular counterpart. This thin-walled ventricle wraps itself around the left ventricle and is most commonly assessed in a qualitative fashion by integrating multiple views (RV inflow– outflow, four-chamber, RV inflow, and transgastric (TG) SAX view). Despite this apparent nonscientific approach to RV function, numerous reports have emerged linking RV function to prognostic outcome in a variety of cardiopulmonary diseases.9 The RV is ideally configured to pump large volumes against a low resistance system. Normal RV measurements can be obtained from a midesophageal four-chamber view at enddiastole (Figure 11.26). Basal measurements at the level of the tricuspid annular plane are normally between 2.0 cm and 2.8 cm, midcavity diameter should not exceed 3.3 cm, and its long axis, measured between the apex and the tricuspid annular plan, should be less than 8 cm.10 RV wall thickness is physiologically less than 5 mm. As opposed to the LV, acute increases in right ventricular afterload are poorly tolerated, leading to RV distension, tricuspid regurgitation, and, ultimately, circulatory collapse. Chronic increases in afterload are compensated by concentric hypertrophy. A semiquantitive method of examining RV function is by interrogating the displacement of the tricuspid annulus toward the RV apex during systole. Under normal circumstances, a descent of 1.5 cm to 2.0 cm should be observed. 3D echocardiography may allow better quantification of RV function. Software programs are emerging showing promising results for their ability to identify the RV endocardial border.

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Figure 11.27. Myocardial segmental model of the left ventricle as reconstructed by software from a 3D dataset. (See Color Plate IX.)

segments of the LV, it is important to grade segment thickening and excursion. Figure 11.26. Midesophageal four-chamber of RV: (1) annular plane measurement, (2) mid-chamber measurement, and (3) long-axis measurement from apex to annular plane.

Assessment of coronary ischemia The ability to reliably detect regional wall motion abnormalities (RWMAs) is clinically relevant because of its diagnostic and therapeutic implications. Not every RWMA detected by TEE is diagnostic for myocardial ischemia. Myocarditis, ventricular pacing, and bundle branch blocks can easily lead to wall motion abnormalities that can potentially lead to mismanagement of the patient. Common classifications should be used to describe the anatomic localization and degree of dysfunction in RWMA, so that communication is possible between echocardiographer and nonechocardiographer, as well as documentation of ongoing disease course. The ASE has published guidelines using a sixteen-segment model of the LV to aid in this communication.11 This model subdivides the LV into three zones (basal, mid, and apical). The basal (segments 1–6) and midventricular zones (segments 7–12) are further subdivided into six segments each, whereas the apical zone consists of only four segments (segments 13–16). Another model, published by the American Heart Association Writing Group on Myocardial Segmentation and Registration for Cardiac Imaging, uses a seventeensegment model. The seventeenth segment merely represents the apical cap of the previously described sixteen-segment model12 (Figure 11.27) The coronary distribution related to the individual segments can be assessed, enabling the echocardiographer to make assumptions regarding the localization of a potential coronary lesion. Segments 1, 2, 7, 13, 14, and 17 are in the distribution territory of the left anterior descending artery. Segments 5, 6, 11, 12, and 16 are associated with the circumflex artery, and segments 3, 4, 9, 10, and 15 belong to the right coronary artery (Figure 11.28). This segmental distribution can be variable among patients owing to the variability of the coronary arteries. In addition to defining a system that defines anatomical

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Wall motion The simplest assessment is achieved by the echocardiographer eyeballing the motion of the ventricle and classifying its motion as being either normal, hypokinetic, akinetic, dyskinetic, or aneurysmal. Subsequently, a numeric score of 1 to 5 can be assigned. A wall motion index can then be derived by dividing the total score by the number of segements observed. A score of 1 would represent a normal ventricle. The higher the score, the more abnormal the ventricle.

Ventricular thickening In addition to movement, the normal myocardium thickens during systole. The degree of thickening can also be used to assess overall function of the observed segment. A thickening less than 30 percent is normal, 10 percent to 30 percent represents mild hypokinesia, 0 percent to 10 percent is severe hypokinesia, no thickening is akinesia, and if the segment bulges during systole, dyskinesia would be present.

Figure 11.28. Sixteen-segment model showing timing and excursion of the individual segments. (See Color Plate X.)

Chapter 11 – Transesophageal Echocardiography

Assessment of pressures and flow Doppler echocardiographic measurements may be used to calculate both flow and pressure gradients. A Doppler spectrum consists of a graph of velocity versus time. If one integrates a given Doppler spectrum over a single cardiac cycle, one may determine the distance traversed over that cardiac cycle. This summation of flow velocities in a given period of time is called the velocity–time integral (VTI). The VTI is represented by the area enclosed within the baseline and spectral Doppler signal. If this distance traversed is multiplied by the cross-sectional area (CSA) of the structure interrogated, one may determine the stroke volume. The CSA of a cylindrical structure can be estimated by the equation: CSA = ␲r 2 ,

(11.4)

where r is the radius of the structure being interrogated. There are a number of assumptions, including (1) laminar blood flow in the area interrogated; (2) a flat or blunt flow velocity profile, such that the flow across the entire CSA interrogated is relatively uniform; and (3) Doppler angle of incidence between the Doppler beam and the main direction of blood flow is less than 20 degrees, so the underestimation of the flow velocity is less than 6 percent. The preferred sites for the measurements of stroke volume are (1) the left ventricular outflow tract or aortic annulus, (2) the mitral annulus, or (3) the pulmonary annulus.13 The major determinant of variability in estimating SV by the use of any technique is the accurate measurement of the CSA. Any error in diameter measurement would be squared in the final results. A second source of variability in measuring aortic flow involves the proper recording of reproducible Doppler signals. If the left ventricular outflow tract (LVOT) is chosen as the CSA, the VTI should be obtained from the Doppler signal at this level. For this purpose, the systolic forward flow must be obtained from either a deep transgastric or a transgastric long axis view. The sample volume of the pulsed Doppler should be placed in the high portion of the LVOT exactly at the same level as the diameter was measured. Occasionally, the Doppler signal is difficult to obtain, and the morphology of the spectrum may be similar to a triangle with a spike at the peak velocity rather than a round bell-shape flow signal. Under such circumstances, it is inappropriate to estimate the VTI, because underor overestimations are likely to result. If attention is given to proper recording techniques, the interobserver variability in measuring the aortic VTI in normal subjects should be less than 5 percent. In an interesting application of echocardiography, various echocardiographic techniques have been used to estimate intracardiac or intravascular pressures. Based on the Doppler shift principle, blood flow velocity can determined. The Bernoulli principle states that an increase in the speed of the fluid occurs simultaneously with a decrease in its pressure or a decrease in the fluid’s potential energy. When flow acceleration and viscous friction variables of blood are ignored and

flow velocity proximal to a fixed obstruction is significantly less than flow velocity after the obstruction, the a simplified modified Bernoulli equation may be defined as: ⌬P = 4v2 ,

(11.5)

where ⌬ P is the pressure difference between two structures, and v is the velocity across the structures. With this formula, the pressure gradient across a fixed orifice can be calculated. The velocity of a regurgitant valve is a direct application of pressure gradient calculations, as it represents the pressure drop across that valve and therefore can be used to calculate intracardiac pressure. For example, tricuspid regurgitation (TR) velocity reflects systolic pressure differences between the RV and right atrium (RA). RV systolic pressure can be obtained by adding RA pressure (estimated or measured) to (TR velocity)2 × 4. In the absence of right ventricular outflow tract obstruction, PA systolic pressure will be the same as right ventricular end systolic pressure (RVESP). For example, If TR velocity = 3 m/s and right atrial pressure (RAP) = 10 mmHg, then, RVESP = (TR VEL)2 × 4 + RAP

(11.6)

RVESP = PA systolic = 4(3)2 = 36 mmHg + 10 mmHg = 46 mm Hg.

Valvular stenosis and regurgitation Aortic valve evaluation Two-dimensional transesophageal echocardiographic interrogation provides information on valve area, leaflet structure, and mobility. The valve is composed of three fibrous cusps (right, left, and noncoronary) attached to the root of the aorta. Each cusp has a nodule called the noduli Arantii in the center of the free edge, at the point of contact of the three cusps. The spaces between the attachments of the cusps are called the commissures, and the circumferential connection of these commissures is the sinotubular junction. The aortic wall bulge behind each cusp is known as the sinus of Valsalva. The sinotubular junction, the sinuses of Valsalva, the valve cusps, the junction of the aortic valve with the ventricular septum, and the anterior mitral valve leaflet comprise the aortic valve complex. The aortic ring is at the level of the ventricular septum and is the lowest and narrowest point of this complex. The three leaflets of the aortic valve are easily visualized, and vegetations or calcifications can be identified on basal transverse imaging or longitudinal imaging.

Aortic stenosis Aortic stenosis may be caused by congenital unicuspid, bicuspid, tricuspid, or quadricuspid valves, rheumatic fever, or degenerative calcification of the valve in the elderly.14 Valvular aortic stenosis is characterized by thickened, echogenic, calcified, immobile leaflets and is usually associated with concentric left ventricular hypertrophy and a dilated aortic root. The valve

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Table 11.1.

Summary of aortic stenosis Aortic sclerosis

Aortic jet velocity (m/sec) Mean gradient (mmHg) Aortic valve area (cm2 )

≤ 2.5

Mild

Moderate

Severe

2.6–2.9 ⬍20 ⬎1.5

3.0–4.0 20–40 1.0–1.5

⬎4.0 ⬎40 ⬍1.0

Adapted from ref. 17.

leaflets may be domed during systole; this finding is sufficient for a diagnosis of aortic stenosis.40 The quantification of aortic stenosis is summarized in Table 11.1. Aortic valve area may be measured by planimetry (Figure 11.29).15 A cross-sectional view of the aortic valve orifice may obtained by TEE, which corresponds well to measurements of aortic valve area obtained by transthoracic echocardiography and cardiac catheterization, assuming the degree of calcification is not severe. The severity of aortic stenosis may be quantified using Doppler echocardiography (Figure 11.30).16 The evaluation of severity, however, may be limited by difficulty aligning the ultrasonic beam with the direction of blood flow through the left ventricular outflow tract. This limitation may be overcome by using either a deep transgastric or transgastric long axis view. Normal Doppler signals across the aortic valve have a velocity of less than 1.5 m/sec and have peak signals during early systole. With worsening aortic stenosis, the flow velocities increase and the peak signal is later in systole. These high velocities will limit the use of pulse wave Doppler and necessitate the use of either continuous wave or high pulse repetition frequency Doppler. Aortic velocity allows classification of stenosis as mild (2.6 to 2.9 m/s), moderate (3.0–4.0 m/s), or severe (⬎4 m/s).17 The higher-velocity central jet is characterized by a highpitched audio sound as well as a fine feathery appearance on the Doppler signal; this is usually less dense than the thicker parajets that are distal to the valve. Peak and mean transvalvular

Figure 11.30. Doppler spectrum through a stenotic aortic valve.

gradients may be calculated using the peak and mean velocities of the signals, respectively. Peak gradients measured by Doppler ultrasonography tend to be higher than those measured in the cardiac catheterization lab, because Doppler-determined peak gradients are instantaneous, whereas those reported by the cardiac catheterization laboratory are peak-to-peak systolic pressure differences. In addition, Doppler determinations of peak gradient may overestimate the gradient because of pressure recovery effects. As blood flows past a stenotic aortic valve, the potential energy of the high-pressure left ventricle is converted into kinetic energy; there is a decrease in pressure with an associated increase in velocity. Distal to the orifice, flow decelerates again with both conversion of this loss of kinetic energy into heat and a reconversion of some kinetic energy into potential energy, with a corresponding increase in pressure. This increase in pressure distal to the stenosis is called the pressure recovery effect.18 Althought they are usually minor, these differences in the observed gradient become more significant with a small aorta and moderate aortic stenosis.19

Figure 11.29. Aortic valve stenosis by planimetry. The panel on the left indicates a normal aortic valve and the right-side panel indicates an aortic valve with stenosis. Because there is no significant calcification of the valve, planimetry may be used.

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Alternatively, aortic valvular area may be calculated using the continuity equation comparing blood flow through the left ventricular outflow tract with blood through the aortic valve. Stroke volume may be estimated by multiplying the crosssectional area of a particular orifice by the VTI over one cardiac cycle through that orifice. The continuity equation states that the calculated stroke volume should be equal independent of the site where it is measured; what goes in must come out. When estimating the severity of aortic stenosis, stroke volume through the left ventricular outflow tract and the aortic valve is usually measured. Using either a deep transgastric or transgastric long axis view, the Doppler spectrum of the aortic valve and left ventricular outflow tract are displayed using continuous and pulse wave Doppler, respectively. The VTI through each of these structures is calculated. The diameter of the left ventricular outflow tract is measured in a midesophageal long axis view. Remembering, SV = CSA × VTI,

(11.7)

where SV = stroke volume, CSA = cross sectional area, and VTI = velocity time integral, the continuity equation states that SVLVOT = SVAV ,

(11.8)

where LVOT = left ventricular outflow tract and AV = aortic valve. Substituting the stroke volume equation into the continuity equation, CSALVOT ×VTILVOT = CSAAV × VTIAV .

(11.9)

Rearranging the terms, CSAAV = CSALVOT × VTILVOT /VTIAV .

(11.10)

Because the left ventricular outflow tract is essentially cylindrical, the CSALVOT may be estimated by CSALVOT = ␲(radiusLVOT )2 .

(11.11)

Because CSALVOT , VTILVOT, and VTIAV are known, the CSAAV or aortic valve area may be calculated. Although multiplane TEE planimetric estimations of aortic valve area may be flawed by heavy aortic valvular calcification, measurements using the continuity equation are accurate compared with Gorlin-derived values.20–21 In a study using TEE, Stoddard and colleagues reported good correlation between aortic valve area measurements using the continuity equation and planimetry; however, they report a steep learning curve for the acquisition of a suitable transgastric long axis view that adequately aligns flow through the aortic valve with the ultrasound beam.22 Mild aortic stenosis is consistent with a valve area greater than 1.5 cm2 , whereas severe stenosis has valve areas less than 1 cm2 .17,23

Aortic regurgitation Aortic regurgitation may be caused by annular dilation, destruction of the annular support, or pathology of the aortic

valvular cusps. Regurgitation secondary to annular dilation is characterized by a dilated aortic root, aortic valve leaflets of normal appearance, and a centrally directed retrograde flow through the left ventricular outflow tract. Valvular lesions that may result in aortic regurgitation include leaflet vegetations and calcifications, perforation, or prolapse. These lesions may be seen on transverse imaging across the aortic valve. Signs that may be associated with aortic regurgitation include highfrequency diastolic fluttering of the MV, premature closing of the MV, or reverse doming of the MV.24–25 Leaflet movement (excessive, restricted, or normal), origin of jet (central or peripheral), and direction of regurgitant jet (eccentric or central) should be determined to provide insight into the underlying pathology.26 Bicuspid and tricuspid valve prolapse is associated with excessive valve mobility and eccentric jet direction and origin. Annular dilation, rheumatic disease, sclerosis, and perforation are associated with normal or reduced cusp mobility and a central jet. Physiological and technical factors may affect estimated severity of aortic regurgitation. Physiological variables may include aortic diastolic pressure, left ventricular end-diastolic pressure, heart rate, and left ventricular compliance.27 The severity of aortic regurgitation may be underestimated in the presence of eccentrically directed jets. Several technical factors affect perceived severity of regurgitation as well, including severe malalignment of ultrasonic planes with blood flow, the presence of a prosthetic MV interfering with ultrasound penetration, gain settings, and pulse repetition frequency. Aortic regurgitant flow through the outflow tract is characteristically a high-velocity turbulent jet extending through the left ventricular outflow tract and LV during diastole. The criteria for qualitative grading of mitral regurgitation are summarized in Table 11.2. The severity of aortic regurgitation may be assessed by examining the area, width, and distal extent of the jet by CFD measurements. Unfortunately, determination of the severity of aortic insufficiency by measurements of regurgitant jet areas alone has been questioned and is probably useful only for distinguishing mild from severe regurgitation.28 A more accurate determination of aortic regurgitation may be made by examination of the width of the origin of regurgitant jet or the ratio of the jet width to the left ventricular outflow tract (wJ /wLVOT ).29–30 A wJ /wLVOT value of 0.25 discriminates mild from moderate regurgitation, and a value of 0.65 discriminates moderate from severe regurgitation.54 A vena contra diameter less than 0.3 cm is consistent with mild aortic insufficiency, and a diameter greater than 0.6 cm is consistent with severe aortic insufficiency. Doppler characteristics of the regurgitant flow may be used to estimate the degree of aortic regurgitation using pressure half-time measurements. A normally functioning aortic valve will maintain a large gradient during diastole between the aorta and the left ventricle. With a small degree of aortic insufficiency, there will be a small volume of blood entering the left ventricle through the aortic valve, resulting in a slow increase in left ventricular pressure during diastole. Doppler measurements will

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Monitoring in Anesthesia and Perioperative Care

Table 11.2.

Quantification of aortic regurgitation

Left atrial size Aortic cusps Jet width in LVOT∗ Continuous wave jet density Jet deceleration rate (pressure half time, ms) Vena contracta width (cm)∗ Jet width/LVOT width, %∗ Jet CSA/LVOT CSA, %∗ Regurgitant orifice area (cm2 )

Mild 1+

Moderate 2+ 3+

Severe 4+

Normal Normal or abnormal Small in central jets Incomplete or faint Slow ⬎ 500

Normal or dilated Normal or abnormal Intermediate Dense Medium 200–500

Usually dilated Abnormal/flail or wide coaption defect Large in central jets; variable in eccentric jets Dense Steep ⬍ 200

⬍ 0.3 ⬍ 25 ⬍5 ⬍ 0.10

0.3–0.60 25–45 46–64 5–20 21–59 0.10–0.19 0.20–0.29

≥ 0.6 ≥ 65 ≥ 60 ≥ 0.30

∗ At Nyquest limits of 50–60 cm/sec CSA = cross-sectional area LVOT = left ventricular outflow tract Adapted from reference 54.

show a regurgitant flow of high velocity, which is maintained during most of diastole (corresponding to a long pressure halftime). As aortic regurgitant flow becomes more severe, there is a more rapid equilibration between aortic and left ventricular diastolic pressure with the nadir of the gradient at end-diastole. As pressures equilibrate, driving pressure across the aortic valve decreases, and Doppler-derived aortic regurgitation velocities decrease over the diastolic period. This pattern of aortic regurgitation flow is characterized by short pressure half-time. Pressure half-time measurements have been validated as a measure of aortic regurgitation.31 A pressure half-time of less than 200 milliseconds is consistent with severe aortic regurgitation, whereas a pressure half-time of more than 500 milliseconds is consistent with mild aortic regurgitation.54 The accuracy of this technique may be influenced by physiologic variables.32 A higher systemic vascular resistance increases the rate of decline, whereas a reduced ventricular compliance will increase the rate of intraventricular pressure rise, which will also affect the diastolic slope without affecting valvular competence. In a given patient, however, pharmacologic manipulation of afterload or inotropy may result in changes in aortic regurgitant slopes and pressure half-times that are contradictory to other measures of regurgitation.

MV primarily supports the posterior MV leaflet, whereas the anterior MV leaflet is continuous with the membranous ventricular septum, aortic valve, and aorta.

Mitral stenosis The most common etiology of mitral stenosis is rheumatic disease; other causes are congenital valvular stenosis, vegetations and calcifications of the leaflets, parachute MV, and annular calcification. In addition to structural valvular abnormalities, mitral stenosis may be caused by nonvalvular etiologies, such as intraatrial masses (myxomas or thrombus) or extrinsic constrictive lesions.35–36 Generally, mitral stenosis is characterized by restricted leaflet movement, a reduced orifice, and diastolic doming (Figure 11.31).37 The diastolic doming occurs when the MV is unable to accommodate all the blood flowing from the left atrium into the ventricle, so the bodies of the leaflets separate more than the edges. In rheumatic disease, calcification of the valvular and subvalvular apparatus, as well as thickening, deformation, and fusion of the valvular leaflets at the anterolateral and posteromedial commissures, produce a characteristic

Mitral valve evaluation The MV consists of two leaflets, chordae tendineae, two papillary muscles, and a valve annulus. The anterior leaflet is larger than the posterior and is semicircular; however, the posterior MV leaflet has a longer circumferential attachment to the MV annulus.33 The posterior valve leaflet may be divided into three scallops: lateral (P1), middle (P2), and medial (P3). The leaflets are connected to each other at junctures of continuous leaflet tissue called commissures. Primary, secondary, and tertiary chordal structures arise from the papillary muscle, subdividing as they extend and attaching to the free edge and several millimeters from the margin on the ventricular surface of both the anterior and posterior valve leaflets.34 The annulus of the

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Figure 11.31. Midesophageal four-chamber view. The mitral valve is severely stenotic, with severe calcification of the annulus and leaflets.

Chapter 11 – Transesophageal Echocardiography

Table 11.3.

Quantification of mitral stenosis

Valve area (cm2 ) Mean gradient (mmHg)

Mild

Moderate

Severe

⬎1.5 ⬍5

1.0–1.5 5–10

⬍1.0 ⬎10

Adapted from reference 17.

fish-mouth–shaped orifice.38 Other characteristics that may be associated with chronic obstruction to left atrial outflow include an enlarged left atrium, spontaneous echo contrast or smoke (which is related to low-velocity blood flow with subsequent rouleaux formation by red blood cells39 ), thrombus formation, and RV dilation. The leaflets, annulus, chordae, and papillary muscles may be assessed in the midesophageal four chamber, commissural, two chamber, and long axis views. If there is significant annular calcification, the transgastric views may be necessary to assess the subvalvular apparatus. Because of the propensity for thrombus formation, the entire left atrium and appendage should be carefully interrogated for thrombus. The assessment of the severity of mitral stenosis is summarized in Table 11.3. Because planimetry of the mitral valve orifice is not influenced by assumptions of flow conditions, ventricular compliance, or associated valvular lesions, its use is the reference standard for the evaluation of mitral valve area in mitral stenosis.17 Although it is at times technically difficult, care should be taken to image the orifice at the leaflet tips. Severe calcification of the MV may interfere with MV area determination and, in patients with significant subvalvular stenosis, underestimation of the degree of hemodynamic compromise may occur when determining the MV area by planimetry.40

Doppler assessment of mitral valvular stenosis A transmitral Doppler spectrum is measured along the axis of transmitral blood flow, which may usually be obtained in a midesophageal four-chamber view or two-chamber view (see Figure 11.32). Transmitral valve flow is characterized by two peaked waves of flow away from the transducer. The first wave

Table 11.4.

(E) represents early diastolic filling, and the second wave (A) represents atrial systole. Transvalvular gradient may be estimated using the modified Bernoulli equation:41 pressure gradient = 4 × velocity2 . Because the peak gradient is heavily influenced by left atrial compliance and ventricular diastolic function, the mean gradient is the relevant clinical measurement.17 The high velocities that may occur with mitral stenosis limit the use of pulse wave Doppler echocardiography; continuous wave Doppler echocardiography should be used. Normally, with the MV opening during early diastole, there is a torrential increase in transmitral flow, which rapidly decreases to zero during diastasis, when the left atrial and ventricular pressures equilibrate. With mitral stenosis, a gradient between the left atrium and ventricle may be maintained for a longer period of time. This sustained pressure differential maintains flow between the atrium and ventricle, decreasing the slope of this early transmitral flow. The rate of decline of the Ewave velocity may be described by its pressure half-time, which is the time interval from the peak E-wave velocity to the time when the E-wave velocity has declined to half its peak value. The pressure half-time is inversely proportional to the mitral valve area:42 Mitral valve area = 220/pressure half-time.

(11.12)

The E wave may have a bimodal characteristic, with an initial rapid decline in transmitral velocity in early diastole compared with the latter aspect of diastole. In these cases, this latter, gentler slope should be measured. The advantage of this technique is that it is independent of valvular geometry. This formula assumes that the mitral valve is at least mildly stenotic. The presence of either mitral regurgitation or aortic regurgitation will decrease the accuracy of pressure half-time measurements for the determination of mitral stenosis.43 If there is associated aortic regurgitation, care should be taken that the aortic regurgitant jet is not included in the transmitral flow measurement.44 Inadvertent inclusion of this aortic regurgitant flow may result in a false elevation of transmitral velocity, as well as a false decrease in pressure half-time.45 Alternatively, aortic insufficiency may result in a rapid increase in diastolic left

Summary of mitral regurgitation

Left atrial size Color flow jet area∗ Pulmonary venous flow Continuous wave jet contour Continuous wave jet density Vena contracta width (cm) Regurgitant orifice area (cm2 )

Mild 1+

Moderate 2+ 3+

Severe 4+

Normal Small central jet (⬍ 4 cm2 or ⬍ 20% LA area) Systolic dominance Parabolic Incomplete or faint ⬍ 0.3 ⬍ 0.20

Normal or dilated

Usually dilated Large central jet (⬎ 10 cm2 or ⬎40% LA) or variable-sized wall impinging jet Systolic flow reversal Early peaking triangular Dense ≥ 0.7 ≥ 0.40

Systolic blunting Usually parabolic Dense 0.3–0.69 0.20–0.29 0.30–0.39

∗ At Nyquest limits of 50–60 cm/sec Adapted from reference 54.

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Figure 11.32. Transmitral Doppler spectrum. The panel on the left is the normal transmitral Doppler flow, and the panel on the right is the transmitral flow in the presence of mitral stenosis.

ventricular pressures, hence decreasing transmitral flow velocity. The continuity equation and proximal isovelocity surface area (PISA) method (discussed later) may be used as secondary methods for the evaluation of the severity of mitral stenosis.

Mitral regurgitation Mitral regurgitation may be caused by disorders of any component of the MV apparatus – specifically, the annulus, the leaflets and chordae, or the papillary muscles. With chronic regurgitation, the annulus and atrium dilate and the annulus loses its normal elliptical shape, becoming more circular.46 Annular dilation, in turn, leads to poor leaflet coaptation and worsening of valve incompetence. Although increased left atrial and ventricular dimensions may suggest severe mitral regurgitation, smaller dimensions do not exclude the diagnosis.47 Ischemic mitral regurgitation is usually the result of left ventricle remodeling and enlargement after prior myocardial infarction. Myxomatous degeneration produces ballooning and scalloping of the valve leaflets as well as localized areas of thinning and thickening, which can be seen echocardiographically. In patients with recent endocarditis, vegetations may be attached to the leaflets or chordae. With rheumatic valve disease, thickening and/or calcification of the leaflets, restriction of the leaflets, and a variable degree of shortening and thickening of the subvalvular apparatus may be identified. Elongated chordae may produce prolapse of one or both attached leaflets; if only one leaflet is affected, leaflet malalignment may occur during systole. Excessively mobile structures near the leaflet tips during diastole may represent elongated chords or ruptured minor chords. These structures do not prolapse into the atrium during systole. In contrast, ruptured major chords are identified as thin structures with a fluttering appearance in the atrium during systole and are associated with marked prolapse of the affected leaflet; in this instance, the valve is said to be flail. A flail leaflet generally points in the direction of the left atrium; this directionality of leaflet pointing is

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the principal criterion for distinguishing a flailed leaflet from severe valvular prolapse.48,49 Flail leaflets are most commonly caused by ruptured chordae and less commonly caused by papillary muscle rupture. Regurgitation may also be caused by papillary muscle infarction in association with infarction of the adjacent left ventricle myocardium, owing to a lack of the normal tethering function performed by these structures. When the adjacent segment is aneurysmal, the dyskinetic wall motion may prevent proper coaptation of the valve by restricting the normal movement of the mitral leaflets during systole.50 Prior infarctions may be indicated by thinning of the myocardium, atresia of the papillary muscles, and dyskinetic wall segments. Atretic papillary muscles are identified by their diminutive size and increased echocardiographic density on short-axis imaging. This shrinkage in papillary muscle size may result in retraction of chordae and subsequent mitral regurgitation. Papillary muscle rupture typically appears as a mass (papillary muscle head) that prolapses into the left atrium during systole and is connected to the leaflet only by its attached chordae. In addition to these structural abnormalities, mitral regurgitation is suggested by left ventricular volume overload, a dilated hypercontractile left ventricle, a high ejection fraction, and systolic expansion of the left atrium.51

Qualitative grading using color flow Doppler The diagnosis of mitral regurgitation is made primarily by the use of color flow mapping. Multiple user adjustable instrument settings (e.g. color Doppler gain, pulse repetition frequency, and filter cutoffs) also influence the apparent size of the CFD jet for any given degree of valvular regurgitation. These settings must be optimized and ideally should be constant when comparing studies on a given patient. Because flow is best detected when it is parallel to the ultrasonic beam and because some mitral regurgitation jets may be thin and eccentric, multiple views of the left atrium should be interrogated for evidence of mitral

Chapter 11 – Transesophageal Echocardiography

the narrowest part of the regurgitant jet at its origin or immediate downstream location. This portion of the jet is known as the vena contracta.59 A vena contracta width of less than 0.3 cm is associated with mild mitral regurgitation, whereas a width greater than 0.7 cm is associated with severe mitral regurgitation. Continuous-wave Doppler integration may also be used in the assessment of the severity of mitral regurgitation.60 A peak velocity that occurs during early systole and is directed toward the left atrium can be appreciated with mitral regurgitation, and the intensity of this recording may be proportional to the severity of regurgitation.61 A dense full signal is associated with severe mitral regurgitation, whereas an incomplete and faint signal is associated with less severe regurgitation. Figure 11.33. Eccentric mitral valve regurgitant jet. (See Color Plate XI.)

Pulmonary vein flow pattern regurgitation. It is important to remember that the regurgitant flow disturbances are 3D velocity fields with complex geometry, which must be sampled from multiple imaging planes to provide an accurate estimate of the maximal spatial extent of the CFD signal. Eccentric jet direction provides corroborative evidence of structural leaflet abnormalities, which may include leaflet prolapse, chordal elongation, chordal rupture, or papillary muscle rupture (Figure 11.33). For example, a jet that is directed laterally along the posterior wall of the left atrium is associated with anterior leaflet prolapse. Similarly, a jet that is directed medially behind the anterior mitral leaflet is associated with prolapse of the posterior leaflet. It is common to detect trivial degrees of mitral valve regurgitation that extend just superior and posterior to the MV leaflet. Mitral regurgitation is detected more frequently by TEE compared with transthoracic imaging, and the degree of regurgitation is often graded as being more severe using TEE.52,53 Atrioventricular valve regurgitation is graded semiquantitatively on a scale of 0 to 4+, where 0 is no regurgitation, 1+ is mild, 2+ is moderate, 3+ is moderate to severe, and 4+ is severe regurgitation. The most common method of grading the severity of mitral regurgitation is CFD mapping of the left atrium. With the Nyquist limits set at 50 to 60 cm/sec, jet areas less than 4 cm2 or 20 percent of the left atrial size are usually classified as mild, whereas jets greater than 10 cm2 or 40 percent of the atrial volume are classified as severe.54 The area of the Doppler jet may be influenced by technical factors such as gain setting, carrier frequency of the transducer, imaging of lowvelocity flows, differentiation of regurgitant from displacement flow, complexities in jet geometry such as multiple jets and vortex flow, temporal variation of jet size during systole, and differences between machines in color Doppler display.55 In addition, jet direction should be considered when grading regurgitation, because eccentric jets that cling to the atrial wall (Coanda effect) have a smaller area than central (free) jets with similar regurgitant volumes and regurgitant fractions.56–58 An alternative method of grading mitral regurgitation is based on the width of

Pulmonary vein flow imaged by transesophageal echocardiography provides useful information regarding regurgitant severity.62 Normally, pulmonary venous flow consists of a phase of retrograde flow during atrial systole, and two phases of antegrade flow during ventricular systole and diastole. Because systolic pulmonary venous flow is augmented by active atrial relaxation, systolic antegrade pulmonary venous flow is usually greater than diastolic antegrade pulmonary venous flow. With mitral regurgitation, there is increased left atrial pressure during ventricular systole, which may either reduce antegrade systolic pulmonary venous flow or cause reversal of systolic flow in cases of severe regurgitation. It is important to interrogate both the right and the left pulmonary veins. With eccentric jets, flow reversal may be more prominent in the pulmonary veins toward which the jet is directed; however, central mitral regurgitation may also result in discordant pulmonary venous flow patterns.63 Although discordant flow occurs primarily with eccentric mitral regurgitant jets with systolic reversal primarily in the right upper pulmonary vein, some patients with central regurgitation may also have discordant pulmonary venous flows.

Proximal isovelocity surface area In addition to these previously discussed indices of mitral regurgitation, regurgitant flow convergence and flow volume also may be used to assess the degree of mitral regurgitation.64 Quantification of mitral regurgitation by PISA assumes that as blood flows toward a regurgitant lesion, flow converges radially. This convergence occurs along increasing isovelocity hemispheres converging on the lesion. Color Doppler may be used to identify these hemispheres of increasing velocity proximal to the lesion (identified by aliasing), and peak flow may be determined by applying the following equation: peak flow = 2␲r 2 vn ,

(11.13)

where r is the radius of the hemispheric spheres and vn is the Nyquist limit.

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Monitoring in Anesthesia and Perioperative Care

Because flow through these isovelocity spheres equals flow through the regurgitant lesion, 2␲r 2 vn = ROAVo ,

(11.14)

where ROA is the area of the regurgitant orifice area and Vo is the maximal velocity. Solving for ROA yields ROA = 2␲r 2 vn /Vo .

(11.15)

Because the regurgitant volume is equal to the area of the regurgitant lesion multiplied by the velocity time integral of the regurgitant velocity (VTIregurg ), Regurgitant volume = VTIregurg (ROA) = VTIregurg (2␲r 2 vn /Vo ).

(11.16)

This method of determining mitral regurgitation is timeconsuming; however, it has been validated as a method of identifying patients with severe mitral regurgitation.65 If the Nyquist limits are set for 40 cm/s and assuming that the patient has “normal” systolic blood pressures (the difference between the systolic left ventricular pressure and left atrial pressure is approximately 100 mmHg), the calculation of ROA may be estimated to be 66

ROA = r 2 /2.

(11.17)

Tricuspid valve The tricuspid valve consists of three leaflets, an annular ring, chordae tendineae, and multiple papillary muscles.67 The anterior leaflet is usually the largest, followed by the posterior and septal leaflets. Chordae arise from a large single papillary muscle, double or multiple septal papillary muscles, and several small posterior papillary muscles, attached to the corresponding walls of the right ventricle. Intrinsic structural abnormalities of the tricuspid valve that can be well characterized by TEE include rheumatic tricuspid stenosis, carcinoid involvement of the tricuspid valve, tricuspid valve prolapse, flail tricuspid valve, Ebstein anomaly, and tricuspid endocarditis. Rheumatic involvement of the tricuspid valve, which is typically seen with concomitant mitral valve involvement, is characterized by thickening of the leaflets (particularly at their coaptation surfaces), fusion of the commissures, and shortening of the chordal structures, resulting in restricted

Table 11.5.

Quantification of tricuspid regurgitation

Right atrial size Tricuspid valve leaflets Jet area – central jets (cm2 )∗ Continuous wave jet density Vena contracta width (cm)∗ PISA radius (cm)∗ Hepatic vein flow ∗ At Nyquist limits of 50–60 cm/s. Adapted from reference 54.

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leaflet motion.68 Carcinoid syndrome results in a diffuse thickening of the tricuspid valve (and pulmonic valve) and endocardial thickening of right heart structures, which may result in restricted tricuspid valve motion (mixed stenosis and regurgitation) of the tricuspid valve.69 The bulky and redundant tricuspid leaflet tissue seen in tricuspid valve prolapse is associated with billowing of leaflet tissue superior to the tricuspid annular plane into the right atrium. In patients with an overtly flail tricuspid valve, the disrupted leaflet tissue wildly prolapses into the right atrium, exhibiting high-frequency systolic vibrations. Destructive processes – such as infective endocarditis, valve trauma induced by inadvertent endomyocardial biopsy of the tricuspid apparatus, and spontaneous rupture of chordae – may all result in a partially flail tricuspid valve apparatus. Supravalvular, valvular, or subvalvular restriction may cause tricuspid stenosis. The most common etiology of tricuspid stenosis is rheumatic heart disease, whereas less common causes include carcinoid syndrome and endomyocardial fibrosis. Tricuspid stenosis is characterized by a domed thickened valve with restricted movement. Tricuspid regurgitation may be secondary to annular or right ventricular dilation or pathology of the leaflets or subvalvular apparatus. Continuous-wave Doppler measurements of the inflow velocities across the tricuspid valve can be employed to estimate the mean diastolic tricuspid valve gradient with the modified Bernoulli equation.70 Optimal alignment of the Doppler cursor parallel to the tricuspid inflow can be difficult to achieve from transesophageal imaging windows. Alignment can often be achieved, however, by positioning the probe deep within the stomach such that the right ventricular apex is imaged at the top of the sector scan. Alternatively, probe positioning at more rostral levels can display the tricuspid valve adjacent to a basal short axis view of the aortic valve (multiplane crystal orientation 25◦ –30◦ ), which may be suitable for continuous-wave Doppler interrogation. Evaluation of the severity of tricuspid regurgitation is frequently required in patients with severe mitral valve disease, severe left ventricular systolic dysfunction and secondary right heart failure, or right ventricular dysfunction resulting from long-standing pulmonary hypertension. The quantification of tricuspid regurgitation is summarized in Table 11.5. The severity of tricuspid regurgitation can be estimated by the apparent size (area in a given imaging plane, volume reconstructed

Mild

Moderate

Severe

Normal Usually normal ⬍5 Soft and parabolic Not defined ≤ 0.5 Systolic dominance

Normal or dilated Normal or abnormal 5–10 Dense, variable contour Not defined, but ⬍ 0.7 0.6–0.9 Systolic blunting

Usually dilated Abnormal/flail or wide coaption defect ⬎10 Dense, triangular with early peaking ⬎0.7 ⬎0.9 Systolic reversal

Chapter 11 – Transesophageal Echocardiography

in three dimensions) of the color flow disturbance of tricuspid regurgitation relative to right atrial size.71 A central jet area of less than 5 cm2 is consistent with mild regurgitation, whereas a jet area greater than 10 cm2 is consistent with severe regurgitation.54 A vena contracta width greater than 0.7 cm is consistent with severe regurgitation.72 The apparent severity of tricuspid regurgitation is exquisitely sensitive to right heart loading conditions. Thus, during the intraoperative evaluation of tricuspid regurgitation, pulmonary artery and right atrial pressures should be kept near levels observed in the awake resting state. To further assist in the evaluation of the hemodynamic significance of tricuspid regurgitation, the hepatic veins can be interrogated from deep gastric positioning of the transesophageal probe. The presence of blunted systolic hepatic vein flow is associated with moderate regurgitation, and retrograde systolic flow is associated with hemodynamically severe tricuspid regurgitation.

Pericardial disease The pericardium is a two-layered structure reflecting from a visceral layer to a parietal layer approximately 1 to 2 cm distal to the origin of the great vessels and around the pulmonary veins. Under normal circumstances, 5 to 10 mL of fluid are contained within the pericardial sac, allowing for practically frictionless motion of the heart during the cardiac cycle. The parietal layer of the pericardium is rich in collagen fibers, making it a lowcompliance structure confining the volume of the four cardiac chambers. In other words, a volume increase in one chamber requires a reduction of volume within another. Likewise, if an increase in volume is seen within the pericardial sac, a reduction of chamber volumes must occur.

Pericardial effusion Under normal circumstances, the echocardiographer is unable to visualize the fluid film between the two layers. Under pathologic conditions fluid accumulation can occur, resulting in the development of a pericardial effusion (Figure 11.24) Typical etiologies leading to pericardial effusions are listed in Table 11.6. Most echocardiographers use a qualitative grading system to characterize the quantity of the pericardial effusion present (minimal, small, moderate, or large). A quantitative score that can be used measures the diameter of the effusion in two dimensions (Table 11.7). Additionally, the effusion can either encompass the entire heart (free effusion) or be loculated. Free effusions are typically seen in medical conditions leading to pericardial effusions, whereas loculated effusions are seen after surgery or inflammatory processes. It is important that the

Table 11.6.

Table 11.7.

Severity of pericardial effusions

Diameter of effusion

Severity

0–0.5 cm 0.6–2.0 cm ⬎2.1 cm

Mild Moderate Severe

echocardiographer pay attention to the anatomical relationship of the effusion. A loculated effusion found primarily at the inferior aspect of the heart can lead to inadvertent injury of the right ventricle if a subxiphoidal approach is chosen for drainage. For the novice echocardiographer, it can be difficult to differentiate a left-sided pleural effusion from a pericardial effusion. A good clue is to identify the descending thoracic aorta. Because the reflection of the pericardium is typically anterior to the descending thoracic aorta, pericardial effusions are generally seen anterior and to the right of the aorta.

Cardiac tamponade Cardiac tamponade and pericardial effusion are not synonymous. A pericardial effusion is an anatomic diagnosis that may or may not lead to hemodynamic alterations. Because of the histologic structure of the pericardium characterized by a thick fibrous tissue, a constraint is exerted on the cardiac chambers within the thorax. Rapid fluid accumulation leads to a sharp rise in pressure within the pericardial sac, because of its low compliance. On the other hand, slow accumulation of fluid can go undetected for long periods of time, resulting in volumes exceeding 1 liter. Under normal circumstances, the respiratory variation of arterial pressure is less than 10 mmHg. During mechanical ventilation, inspiratory positive pressure leads to impeded rightsided filling of the heart. The increase in intrathoracic pressure reduces the capacity of the pulmonary veins and augments the filling of the left side of the heart. During expiration, the exact opposite occurs. As the pressure increases within the pericardial sac, the total blood volume within the heart becomes limited, leading to an exaggerated response to the respiratory cycle. If the pressure of the intrapericardial fluid is not relieved, an equalization will occur among diastolic pressures within the heart. Echocardiographically, this can be identified as a right ventricular collapse during diastole, as well as a right atrial collapse during systole. More subtle signs of pericardial tamponade can be detected with Doppler-based modalities. A respiratory variation of more than 30 percent in peak transmitral or transtricuspid valve flow velocity represents a typical finding.

Etiologies of pericardial effusions

Idiopathic

Infections

Inflammatory

Post- myocardial infarction

Systemic disease

Malignancy

Miscellanous

Acute Chronic

Viral Bacterial Fungal

Lupus Rheumatoid arthritis

Dressler syndrome Acute after transmural infarct

Uremia Cirrhosis Hypothyroidism

Direct Lymphatic obstruction

Posttrauma Postsurgical CHF

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This can be achieved by positioning the pulse wave gate just at the leaflet tips of the mitral or tricuspid valve. Although a large pericardial effusion is frequently associated with pericardial tamponade, other etiologies can also be responsible for respiratory variation in transvalvular flow velocities (e.g. high airway pressures, hematoma).

Aortic disease Because of the intimate anatomic relationship between the aorta and the esophagus, TEE has proved to be useful in the diagnosis of aortic dissection and aortic atherosclerosis. Detailed reviews of TEE diagnosis of these diseases have recently been published.73,74 In the diagnosis of aortic dissection, TEE has overcome some of the major disadvantages of the alternative diagnostic modalities (CT, MRI). In comparison to these modalities, TEE has been shown to have high sensitivity and specificity.75,76 An examination can be performed within about 15 to 20 minutes, and a diagnosis can usually be obtained at the same time. The diagnosis is based on the presence of an intimal flap. Ideally, the specific locations of the entry and exit sites are also identifiable. Flow in both the true and false lumina can be analyzed with Doppler color flow imaging. TEE is performed in real time, allowing for its unique ability to give functional and hemodynamic information. This enables the detection of the common complications of aortic dissection: aortic valve regurgitation, pericardial tamponade, and left ventricular dysfunction secondary to coronary artery involvement in the dissection process. In addition to the common sequelae of aortic dissection, TEE can also identify a rare but potentially lethal complication of aortic intimal intussusception.77 Neurologic injury after cardiopulmonary bypass remains a devastating complication of cardiac surgery. Possible etiologies include hypoperfusion, lack of pulsatile flow, and cerebral embolization of gaseous or particulate matter. The thoracic aorta is a potential source of such emboli, as it often contains atherosclerotic plaques and it may be instrumented multiple times during cardiac operations. TEE can also be used to detect aortic intraluminal thrombi and plaques. One major limitation is that the distal ascending and proximal transverse aortas are not well visualized by TEE.78 Although the entire ascending aorta is not well visualized, TEE can serve as a screen to detect aortic atherosclerotic debris.79 The presence of atherosclerotic disease in the visualized portions increases the likelihood of finding atherosclerotic changes in the nonvisualized portion of the aorta. Intraoperatively, this region can be scanned by placing a sterile wrapped probe directly on the aorta to rule out pathology in the locations of planned instrumentation. Once the disease is defined, it can often be avoided during instrumentation and hopefully neurologic injury can be prevented. This epiaortic scanning is more sensitive than digital palpation in the detection of atherosclerotic disease, and its use has modified surgical management during cardiac surgery.80 Although epiaortic scanning may be justified for all patients presenting

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for cardiac surgery, its use should be seriously considered in those patients with increased risk for embolic stroke, including patients with a history of cerebrovascular or peripheral vascular disease or patients with evidence of aortic disease by any modality.81 Phase array probes are generally used for perioperative aortic scanning. Because of the fan-shaped sector displayed, the most anterior aspect of the aorta cannot be adequately visualized unless a standoff is used between the transducer and the aorta. It is usually most convenient to fill the pericardial cradle with saline and hold the probe approximately 1 cm anterior to the aorta while scanning. A complete examination will include short axis views of the proximal, middle, and distal ascending aorta and long axis views of both the ascending aorta and arch. These views will allow for evaluation of the twelve areas of the aorta: anterior, posterior, and left and right lateral walls of the proximal, middle, and distal ascending aorta. The proximal ascending aorta is defined as the region from the sinotubular junction to the proximal intersection of the right pulmonary artery. The middle ascending aorta includes the portion of the aorta that is adjacent to the right pulmonary artery. The distal ascending aorta extends from the distal intersection of the right pulmonary artery to the origin of the innominate artery. The severity of atherosclerosis may be graded according to the classification described by Katz and coworkers and is summarized in Table 11.8.82

Practice parameters and evidence of utility An updated report by the American Society of Anesthesiologists (ASA) and the Society of Cardiovascular Anesthesiologists (SCA) Task Force on Transesophageal Echocardiography is currently available on the Internet and should be published shortly.83 This document updates the 1996 published guidelines for the perioperative use of TEE.84 The update currently recommends that perioperative TEE should be used in all adult patients who have no contraindications for TEE and present for cardiac or thoracic aortic procedures. A complete TEE exam should be performed in all patients with the following intent: (1) confirm and refine the preoperative diagnosis, (2) detect new or unsuspected pathology, (3) adjust the anesthetic and surgical plan accordingly, and (4) assess results of the surgical intervention. For patients presenting to the catheterization laboratory, the use of TEE may be beneficial. Especially in the setting of Table 11.8.

Quantification of aortic atherosclerotic disease

Grade

Description

I II III IV V

Normal to mild intimal thickening Severe intimal thickening without protruding atheroma Atheroma protruding ⬍ 5 mm into lumen Atheroma protruding ≥ 5 mm into lumen Any thickness with mobile component or components

Adapted from reference 82.

Chapter 11 – Transesophageal Echocardiography

catheter-based valve replacement and repair and transcatheter intracardiac procedures, both consultants and ASA members agreed that TEE should be used. In the setting of noncardiac surgery, TEE may be beneficial in patients with known or suspected cardiovascular pathology, which potentially could lead to severe hemodynamic, pulmonary, or neurologic compromise. In life-threatening situations of circulatory instability, TEE remains indicated. A similar viewpoint is taken by the consultants and ASA members in regard to critically ill patients. TEE should be used to obtain diagnostic information that is expected to alter management in the ICU, especially when the quality of transthoracic images is poor or other diagnostic modalities are not obtainable in a timely manner. The perioperative use of TEE may improve outcome. Eltzschig and associates reported that 7 percent of 12,566 consecutive TEE exams directly influenced surgical decisionmaking.85 Combined procedures (CABG, valve) were most commonly influenced by perioperative TEE. In 0.05 percent, the surgical procedure was actually canceled as a direct result of the intraoperative TEE exam. Minhaj and colleagues looked at a much small cohort and found that in 30 percent of patients, the routine use of TEE during cardiac surgery revealed a previously undiagnosed cardiac pathology, leading to change in surgical management in 25 percent of patients studied.86

Complications and contraindications Complications resulting from intraoperative TEE can be separated into two groups: injury from direct trauma to the airway and esophagus, and indirect effects of TEE. In the first group, potential complications include esophageal bleeding, burning, tearing, dysphagia, and laryngeal discomfort. Further confirmation of the low incidence of esophageal injury from TEE is apparent in the few case reports of complications. A study of 10,000 TEE examinations yielded one case of hypopharyngeal perforation (0.01%), two cases of cervical esophageal perforation (0.02%), and no cases of gastric perforation (0%).87 Kallmayer and associates reported an overall incidences of TEE-associated morbidity and mortality of 0.2 percent and 0 percent, respectively. The most common TEE-associated complications was severe odynophagia, which occurred in 0.1 percent of the study population, followed by dental injury (0.03%), endotracheal tube malpositioning (0.03%), upper gastrointestinal hemorrhage (0.03%), and esophageal perforation (0.01%).88 Piercy and colleagues have reported a gastrointestinal complication rate of approximately 0.1%, with a greater frequency of injuries among patients more than 70 years old and among women. If resistance is met while advancing the probe, the procedure should be aborted to prevent these potentially lethal complications. Another possible complication of esophageal trauma is bacteremia. Studies have shown that the incidence of positive blood cultures in patients undergoing upper gastrointestinal endoscopy is 4 to 13 percent, 89,90 and that in patients undergoing TEE it is 0 to 17 percent. 91–93 Even though bacteremia may

occur, it does not always cause endocarditis. Antibiotic prophylaxis in accordance with the American Heart Association guidelines is not routinely recommended but is optional in patients with prosthetic or abnormal valves, or who are otherwise at high risk for endocarditis.94 The second group of complications that result from TEE includes hemodynamic and pulmonary effects of airway manipulation and, particularly for new TEE operators, distraction from patient care. Fortunately, in the anesthetized patient there are rarely hemodynamic consequences to esophageal placement of the probe, and there are no studies that specifically address this question. More important for the anesthesiologist are the problems of distraction from patient care. There have been instances in which severe hemodynamic and ventilatory abnormalities have been missed because of fascination with the images or the controls of the echocardiograph machine. To ensure the continued safety of TEE, the following recommendations are made: The probe should be inspected prior to each insertion for cleanliness and structural integrity. If possible, the electrical isolation should also be checked. The probe should be inserted gently and, if resistance is met, the procedure aborted. Minimal transducer energy should be used and the image frozen when not in use. Finally, when not imaging, the probe should be left in the neutral, unlocked position to prevent prolonged pressure on the esophageal mucosa. Absolute contraindications to TEE in intubated patients include esophageal stricture, diverticula, tumor, recent suture lines, and known esophageal interruption. Relative contraindications include symptomatic hiatal hernia, esophagitis, coagulopathy, esophageal varices, and unexplained upper gastrointestinal bleeding. Despite these relative contraindications, TEE has been used in patients undergoing hepatic transplantation without reported sequelae.95,96

Credentialing This is an era in medicine in which the observance of guidelines for training, credentialing, certifying, and recertifying medical professionals has become increasingly common. Although there have been warnings97 and objections98 to anesthesiologists making diagnoses and aiding in surgical decision making, there is no inherent reason that an anesthesiologist cannot provide this valuable service to the patient. The key factors are proper training, extensive experience with TEE, and available backup by a recognized echocardiographer. In 1990, a task force from the American College of Physicians, the American College of Cardiology (ACC), and the American Heart Association (AHA) created initial general guidelines for echocardiography.99 The ASE also provided recommendations for general training in echocardiography and has introduced a self-assessment test for measuring proficiency. These organizations recommended the establishment of three levels of performance with a minimum number of cases for each level – level 1: introduction and an understanding of the indications (120 2D and 60 Doppler cases); level 2:

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Monitoring in Anesthesia and Perioperative Care

independent performance and interpretation (240 2D and 180 Doppler cases); and level 3: laboratory direction and training (590 2D and 530 Doppler cases).98,100 However, these guidelines are limited because they are not based on objective data or achievement. Furthermore, because different individuals learn at different rates, meeting these guidelines does not ensure competence, nor does failure to meet these guidelines preclude competence. Proficiency in echocardiography can be achieved more efficiently in a limited setting (i.e. the perioperative period) with fewer clinical applications (e.g. interpreting wall motion, global function, and mitral regurgitation severity) than in a setting that introduces every aspect of echocardiography. The ASA and the SCA have worked together to create a document on practice parameters for perioperative TEE.101 The SCA then created a Task Force on Certification for Perioperative TEE to develop a process that acknowledges basic competence and offers the opportunity to demonstrate advanced competence, as outlined by the SCA/ASA practice parameters. This process resulted in the development of the Examination of Special Competence in Perioperative Transesophageal Echocardiography (PTEeXAM). In 1998, the National Board of Echocardiography was formed. Currently, board certification in perioperative transesophageal echocardiography may be granted by meeting the following requirements: (1) the holding of a valid license to practice medicine, (2) board certification in an approved medical specialty (e.g. anesthesiology), (3) training and/or experience in the perioperative care of surgical patients with cardiovascular disease, (4) the study of 300 echocardiographic examinations, and (5) the passing of the PTEeXAM.102

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patients with aortic dissection. J Thorac Cardiovasc Surg 1992;103:1113–8. Hudak A, Konstadt SN. Aortic intussuception: A rare complication of aortic dissection. Anesthesiology 1995;82:1292–4. Konstadt SN, Reich DL, Quintana C, Levy M.The ascending aorta: how much does transesophageal echocardiography see? Anesth Analg 1994;78:240–4. Konstadt SN, Reich DL, Kahn R, Viggiani RF. Transesophageal echocardiography can be used to screen for ascending aortic atherosclerosis. Anesth Analg 1995;81:225–8. Djaiani G, Ali M, Borger MA, Woo A, et al. Epiaortic scanning modifies planned intraoperative surgical management but not cerebral embolic load during coronary artery bypass surgery. Anesth Analg 2008;106:1611–8. Glas KE, Swaminathan M, Reeves ST, et al. Guidelines for the performance of a comprehensive intraoperative epiaortic ultrasonographic examination: recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists; endorsed by the Society of Thoracic Surgeons. Council for Intraoperative Echocardiography of the American Society of Echocardiography; Society of Cardiovascular Anesthesiologists; Society of Thoracic Surgeons. Anesth Analg 2008;106:1376–84. Katz ES, Tunick PA, Rusinek H, Ribakove G, Spencer FC, Kronzon I. Protruding aortic atheromas predict stroke in elderly patients undergoing cardiopulmonary bypass: experience with intraoperative transesophageal echocardiography. J Am Coll Cardiol 1992;20:70–7. http://www.asahq.org/clinical/TEE PracticeGuidelinesUpdate. pdf. Accessed May 13, 2009. Practice Guidelines for Perioperative Transesophageal Echocardiography. Anesthesiology 199;84(4):986–100. Eltzschig HK, Rosenberger P, L¨offler M, Fox JA, Aranki SF, Shernan SK. Impact of intraoperative transesophageal echocardiography on surgical decisions in 12,566 patients undergoing cardiac surgery. Ann Thorac Surg 2008;85(3): 845–52. Minhaj M, Patel K, Muzic D, et al. The effect of routine intraoperative transesophageal echocardiography on surgical management. J Cardiothorac Vasc Anesth 2007;21(6):800–4. Min JK, Spencer KT, Furlong KT, et al. Clinical features of complications from transesophageal echocardiography: a single-center case series of 10,000 consecutive examinations. J Am Soc Echocardiogr 2005;18:925–9. Kallmeyer IJ, Collard CD, Fox JA, et al. The safety of intraoperative transesophageal echocardiography: a case series of 7200 cardiac surgical patients. Anesth Analg 2001;92:1126–30. Everett ED, Hirschman JV. Transient bacteremia and endocarditis prophylaxis. Medicine 1977;56:61. Botoman VA, Surawicz CM. Bacteremia with gastrointestinal endoscopic procedures. Gastrointest Endosc 1986;32:342. Nikutta P, Mantey-Stiers F, Becht I, et al. Risk of bacteremia induced by transesophageal echocardiography: analysis of 100 consecutive procedures. J Am Soc Echocardiogr 1992;5:168. Melendez LJ, Kwan-Leung Chan, Cheung PK, et al. Incidence of bacteremia in transesophageal echocardiography: a prospective study of 140 consecutive patients. J Am Coll Cardiol 1991;18:1650. Steckelberg JM, Khandheria BK, Anhalt JP, et al. Prospective evaluation of the risk of bacteremia associated with transesophageal echocardiography. Circulation 1991;84:177.

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94. Dajani AS, Bisno AAL, Chung KJ, et al. Prevention of bacterial endocarditis. JAMA 1990;264:2919. 95. Ellis JE, Lichtor JL, Feinstein SB, et al. Right heart dysfunction, pulmonary embolism, and paradoxical embolization during liver transplantation. Anesth Analg 1989;68:777. 96. Suriani RJ, Cutrone A, Feierman D, Konstadt S. Intraoperative transesophageal echocardiography during liver transplantation. J Cardiothorac Vasc Anesth 1996;10:699–707. 97. Kaplan JA. Monitoring technology: advances and restraints. J Cardiothorac Anesth 1989;3:257. 98. Pearlman AS, Gardin JM, Martin RP, et al. Guidelines for physician training in transesophageal echocardiography: recommendations of the American Society of Echocardiography. J Am Soc Echocardiogr 1992;5:187.

99. Popp RL, Williams SV, Achord JL, et al. ACP/ACC/AHA Task Force on Clinical Privileges in Cardiology: Clinical competence in adult echocardiography. J Am Coll Cardiol 15:1465–1468, 1990. 100. Pearlman AS, Gardin JM, Martin RP, et al. Guidelines for optimal physician training in echocardiography. Recommendations of the American Society of Echocardiography Committee for Physician Training in Echocardiography. Am J Cardiol 1987;60:158–63. 101. Thys D, Abel M, Botlen B, et al. Practice parameters for intraoperative echocardiography. Anesthesiology 1996;84:986–1006. 102. http://www.echoboards.org/certification/pte/reqs.html. Accessed December 18, 2008.

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12

Ultrasound guidance of vascular catheterization Andrew B. Leibowitz and Jonathan Elmer

Technical concepts The basic principles of ultrasound are covered in Chapter 11, but for the sake of completion they will be re-reviewed here. There are two basic kinds of ultrasound applicable to vascular access, Doppler and B-mode (also known as two-dimensional [2D]). The Doppler principle may be used to determine the velocity of moving objects, such as red blood cells within a vessel. This velocity information may be displayed as a velocity-versus-time spectrum or may be converted into an audio signal, in which different velocities are rendered as different pitches. Anesthesiologists are most familiar with this technique when it is used to “hear” a pulse to measure blood pressure or the presence or absence of circulation in an extremity (e.g. following vascular bypass). Signals obtained from arteries and veins sound distinctively different and thus can be used to help assist in the identification of vascular structures. Doppler ultrasound can be used alone or combined with 2D ultrasound. With the exception of color Doppler, Doppler ultrasound alone is currently rarely used to assist in vascular catheterization. B-mode or 2D ultrasound renders reflected ultrasound signals into a 2D gray-scale image. B stands for brightness. Signals returning to the transducer are assigned a gray scale based on amplitude. The device’s contrast resolution determines the number of shades of gray that are displayed. Fluidfilled structures (e.g. blood, fluid in collections) are echolucent and are shown as dark gray or black; soft tissue (e.g. muscle) is more echogenic and appears gray; and solid structures (e.g. thick tendons, bone) are very echogenic and appear white (Figure 12.1). When applied to vascular access, a key use of ultrasound is the identification of and differentiation between arterial and venous structures. Vascular structures can be further assessed by their overall shape and, of greater importance, compressibility. Patent veins are much more compressible and can often be collapsed with the application of pressure, unlike arteries, which retain much of their original shape and appearance. Extrathoracic veins will also enlarge more than arteries with Valsalva maneuvers and Trendelenburg positioning. Finally, the pulsatility of arterial structures can be visualized; however, because this pulsation can be transmitted to adjacent structures, extra care must be taken to avoid confusion.

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These devices are used in two main ways: static and dynamic imaging. In static imaging, the anatomy is defined and an “x marks the spot” technique is applied. These authors highly recommend against this technique, because the relative relationship between surface and deep anatomy can change dramatically with minor changes in positioning that may occur between the marking and start of the procedure (Figure 12.2)1–3 . We recommend dynamic imaging, whereby the transducer is covered in a sterile sheath and held in the nondominant hand and the needle stick is performed with the dominant hand. Other important technical points that are frequently overlooked include the following: 1. The proper orientation of the transducer should be verified at the beginning of the procedure to ensure that pressure on the left side of the transducer is visualized on the left side of the screen. The recommended transducer orientation is not always clearly marked on the probe. 2. The screen should be positioned in a comfortable place so the operator can see it within a 30-degree glance from the operative field. This positioning will allow almost simultaneous visualization of the surface anatomy and the monitor. When performing an internal jugular catheterization, we prefer the screen to be located on the ipsilateral side of the bed, approximately within arm’s reach (Figure 12.3). 3. Ultrasound jelly must be placed within the condom sheath and on the skin to obtain an adequate image. 4. Always start by positioning the vein in the center of the screen and adjust the depth monitored so that the entire needle path can be visualized easily. 5. Pay attention to the actual depth of the vessel by noting the ruler on the screen or the actual size of the image that is rendered, in centimeters. Knowledge of depth will help prevent the operator from accidentally entering the pleural space. The transducer can be manipulated in several ways to optimize the image and acquire the most information. The four basic maneuvers are pressure, alignment, rotation, and tilting; they can be remembered with the acronym PART. Short axis and long axis techniques may be used (Figure 12.4), but the short axis approach is more commonly preferred. Some devices

Chapter 12 – Ultrasound Guidance of Vascular Catheterization

Figure 12.1. Picture obtained from the ultrasound image of the right neck of a patient. The vein lies lateral to the artery in this patient, is larger, and is not as circularly shaped.

A

A

V

A

B A

V A

V

V

A V

A

V

Figure 12.2. Figure demonstrating the effect of change in head position on overlap of the vein and artery. From reference 1, with permission.

Figure 12.4. Short and long axis views of the internal jugular vein.

Figure 12.3. Ideal positioning of patient, operator, and monitor. This photo depicts a preprocedure scan of the left internal jugular vein. The transducer is held in the nondominant hand, and the monitor is on the ipsilateral side of the planned procedure, as close to the midline of the operative field as possible.

allow the simultaneous visualization of both images, which can be quite helpful to the experienced operator, but, in our experience, confuses the novice operator. Long axis views will allow the experienced operator to visualize the entire needle along its plane of passage into the vessel; however, the artery and vein will often not be visualized in the same long axis image. Vigilance must be maintained to avoid confusing the artery with the vein. In contrast, the short axis view almost always allows continuous visualization of both the artery and the vein. There are many ultrasound machines and transducers available. The larger, more complicated, machines are almost always capable of performing vascular ultrasound if configured properly. Only a few systems are designed specifically for vascular catheterization. The main determinant factor of suitability for vascular imaging is the frequency of the transducer. High frequencies are associated with better resolution of the vascular structures. Vascular ultrasound should generally be performed with a 7.5- to 10-MHz linear array transducer. This transducer

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device that can be sheathed and placed into the operative field. This will allow the operator to work independently. 5. The ability to print or store images will be germane to documentation, performance improvement efforts, and billing. 6. A storage basket on the device pole to hold the sheaths, gels, and other extraneous equipment, such as printer paper, is necessary. Although devices that incorporate more features almost always appear to be more desirable, the authors feel that if the device will be used only for vascular catheterization, a simpler device with fewer features and controls not only will allow more rapid skill acquisition and acceptance, but will also cost less and be less likely to need repair. Figure 12.5. Three transducers that the author (ABL) uses. On the left is the Bard Site Rite 3, in the middle is the SonoSite iLook, and on the right is the SonoSite S-ICU. Note the differences in shape and width.

has a flat face, resulting in a rectangular image that allows adequate visualization of the vasculature structures of interest, their depth, and their relationship to immediately adjacent structures. Unlike the phase array probes, linear array probes have minimal near-field dropout, which allows for visualization of very superficial structures. Color Doppler will further enhance the ability to differentiate arteries from veins and is now commonly available in several devices, but it is not absolutely necessary. Of note, the color assigned in Doppler views (traditionally, either red or blue) represents only the direction of flow relative to the transducer. Thus, a vein may be depicted as either red or blue, as may an artery, depending on the angulation of the transducer. The transducer should not be too large, as this will interfere with its ability to fit into the operative field, especially in pediatric patients, and in adults if the neck is particularly short and fat. The shape of transducers varies tremendously; the operator should make sure to be comfortable holding it in his or her nondominant hand (Figure 12.5). When purchasing a vascular ultrasound device, consider several important aspects of the monitor and the stand: 1. The device size and portability, especially the footprint of the stand, will determine whether it can be used in tight quarters. Space requirements may vary greatly from one work area to another. 2. The device should function on alternating current or with a battery. Battery life may be important if the device will travel away from a home base for long periods. 3. Larger screens allow the image to be magnified. This feature is helpful when the vasculature is small. 4. The layout of control functions varies tremendously from device to device. One particularly helpful advance is the presence of controls to adjust gain, image magnification, and depth on the transducer itself, or on a remote control

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Parameters monitored We recommend a preprocedure examination before prepping and draping the selected site. Important information obtained from a preprocedure examination should include at least the following: 1. The absolute presence of the intended target vessel is established. 2. The vessel’s size should be estimated. 3. The vein’s relationship to the artery should be carefully noted, particularly what percentage overlay there is and whether the amount of overlay can be improved by turning the head. 4. The presence of echogenic material within the vessel suggestive of clot or thrombus should be determined. Similarly, complete or nearly complete compressibility of the vessel should be observed to rule out venous thrombosis. 5. How the vessel changes in size with Trendelenburg positioning and Valsalva maneuver should be noted. 6. If any of the previous issues presents concern, then other potential sites should be similarly interrogated. Prior vascular catheterizations may have scarred, stenosed, or thrombosed the target vessel; a preprocedure examination may immediately lead to change of site. If the vein appears small despite steep Trendelenburg positioning and Valsalva maneuver, or its anatomy relative to the artery is unsatisfactory and arterial puncture is perhaps unavoidable, imaging of the other side should be performed and the comparable risk of the two sides weighed. At the very least, if the first site chosen is unsuccessful, the likelihood of success in the backup site could be estimated a priori. Imaging will help the clinician communicate to the patient the potential for increased difficulty, multiple punctures, and failure. Prior warning of these adverse events seems to increase patient satisfaction. When the dynamic technique is used, the vessel is visualized in real time. When local anesthetic is injected, the needle should be visualized in the expected plane of approach and the formation of an echogenic local anesthesia bubble anterior to

Chapter 12 – Ultrasound Guidance of Vascular Catheterization

the vessel should be appreciated. If the vessel is small, coaching the patient to Valsalva or steepening the Trendelenburg position will be helpful. The needle should be seen to invaginate the anterior wall of the vessel and usually can be seen to enter the vessel if the relative planes of the transducer and needle tip are correctly oriented. The guidewire may be visualized within the vessel lumen. If catheterization is unsuccessful, the vessel may disappear and ultrasonic evidence of hematoma formation may be appreciated. This information may lead to the abandonment of that site in a timely fashion, which will reduce time, discomfort, and potential for complications. Preprocedural examination will also have allowed for a thoughtful and orderly progression of attempts at an alternative site or the decision to abort the procedure completely.

Evidence of utility Traditional approaches Historically, central venous catheter (CVC) insertion has been performed by blind techniques that rely on anatomic landmarks such as the sternocleidomastoid muscle heads and carotid pulse (internal jugular [IJ] cannulation), the bend of the clavicle (subclavian cannulation), or the inguinal ligament and femoral pulse (femoral cannulation). Such techniques require knowledge of regional anatomy and assume that this anatomy is readily identifiable and invariant from patient to patient. Landmarkbased techniques are generally viewed as safe and effective when performed by an experienced operator in optimal conditions. However, historical data show overall noninfectious complication and failure rates as high as 40 percent in adult patients.2–6 Failure can be attributed to three major factors: patient-related factors, anatomic variability, and operator inexperience. Numerous patient-related factors have been associated with increased risks of complications from CVC placement. These factors include lack of traditional anatomic landmarks in morbid obesity, extremes of age, or previous radiation or surgery that distorts normal anatomy; factors that increase risk of bleeding with arterial puncture, such as coagulopathy or thrombocytopenia; and factors that limit the patient’s ability to tolerate mechanical complications of insertion, such as decreased cardiopulmonary reserve.4,5 Not surprisingly, pediatric patients are generally at higher risk for almost all major complications.7,8 Even in a patient without specific risk factors for difficult cannulation, intrinsic anatomic variability often leads to poor outcomes. This variability is best demonstrated by the example of IJ CVC insertion. The landmark technique for IJ cannulation relies on identification of the two heads of the sternocleidomastoid and/or the carotid pulse; the needle is inserted at the apex of the two heads lateral to the palpated pulse. This technique assumes a lateral location of the jugular vein relative to the carotid artery, an assumption only true in a minority of patients (Figure 12.6).2 In fact, in most cases, the jugular vein

Figure 12.6. Figure demonstrating the relative position of the vein to the carotid artery (CA) compiled from several studies. From reference 2, with permission.

overlaps the carotid artery anteriorly to at least some extent, and may even lie medial to the artery. Operator experience also plays a significant role in the complication and failure rates of the landmark technique.5,9 We suggest that approximately 50 line placements are required before an operator can be deemed competent to place CVCs independently. Operators who have placed more than 50 lines have half the complication rate of those who have placed fewer than 50.

Ultrasound guidance Because of the relatively high complication rate of landmarkbased CVC placement, as discussed previously, the development of ultrasound-guided techniques for CVC was greeted with considerable excitement. As discussed elsewhere in this chapter, three broad categories of ultrasound guidance for central venous catheterization exist: Doppler, 2D static, and 2D dynamic. Doppler, although initially thought to be promising, proved to be inferior to 2D ultrasound guidance and equivalent to landmark techniques in a majority of studies in both adult and pediatric populations.10–13 As a consequence, the technique has largely been abandoned. Static ultrasound has been compared with dynamic ultrasound and landmark techniques in several moderate-sized randomized controlled trials in recent years (Table 12.1). Because of the few studies that directly compare static ultrasound to another technique, conclusions about its utility are limited; however, static ultrasound was demonstrated to be superior to landmark in one adult and one pediatric study.14,15 Data comparing dynamic ultrasound with static ultrasound are equivocal, with dynamic ultrasound appearing to be superior to static ultrasound in several studies, and equivalent in others.15–17 Of note, to date there are no studies suggesting statistical or nonsignificant trend toward superiority of static ultrasound. However, additional studies are required to elucidate significant differences between the two. In contrast with static ultrasound, numerous clinical trials have demonstrated the efficacy of dynamic ultrasound guidance in CVC placement in a variety of clinical settings and patient populations, both adult (Table 12.2) and pediatric (Table 12.3). In the overwhelming majority of studies, dynamic

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Table 12.1.

Studies of static ultrasound prelocation in adult and pediatric populations

First Author/ Year

Study Type Comparison

Chuan 200514 Hosokawa 200716 Milling 200515 Hayashi 200217 Hayashi 200217

RCT SUS vs LM RCT DUS vs SUS RCT DUS vs SUS vs LM RCT DUS vs SUS RCT DUS vs SUS

Patient type

n

Total success

Mean Attempts

Complications1

Conclusions

Infants ⬍12 kg

62

80% vs 100%

2.55 vs 1.57

26.7% vs 3.1%

Infants ⬍7.5 kg

60

89% vs 100%NS

NR

4% vs 0%NS

Adults

201

5.2 vs 2.9 vs 2.32

13% vs 3% vs 3%

Adults w/ VAD

188

64% vs 82% vs 98% 96.9% vs 97.6%NS

NR

1% vs 3.3%NS

Adults w/o VAD

53

78.3% vs 97.6%

NR

13% vs 0%

Benefit to SUS over LM in peds NS trend favoring DUS over SUS in peds DUS better than SUS better than LM in adults DUS equivalent to SUS if VAD DUS superior to SUS if no VAD

NS

Abbreviations: RCT = randomized controlled trial; LM = landmark; SUS = static ultrasound prelocation; DUS = real-time dynamic ultrasound; VAD = ventilatorassociated venodilation; NR= not reported; Peds = pediatrics; NS, not significant. 1 Major complications unless otherwise noted (arterial puncture, pneumothorax, hemothorax). 2 All significant except DUS vs SUS.

ultrasound use increased overall success rates, decreased the number of attempts required for cannulation, and reduced the number of mechanical complications associated with CVC placement. In addition to these general studies, the limitations of landmark techniques described previously have prompted Table 12.2.

several investigators to examine the safety and efficacy of dynamic ultrasound in a variety of high-risk patient populations (Table 12.4). In each of these patient populations, dynamic ultrasound has been demonstrated to be safe, effective, and superior to landmark techniques.

Studies of dynamic ultrasound use compared with landmark technique in adult populations

First author/Year Gualtieri 199536 Karakitsos 200637 Leung 200638 Mallory 199039 Milling 200640 Troianos 199141 Hilty 199742 Miller 200243 Cajozzo 200444 Hrics 199845 Wigmore 200746 Augoustides 200247 Martin 200448 Cajozzo 200449

Study type Site (if not IJ) RCT Subclavian RCT RCT RCT RCT RCT Randomized case-control Femoral Prospective quasi-random3 Prospective quasi-random5 Prospective case series Prospective case series Prospective case series Prospective case series Retrospective chart review

Setting Patient population ICU

n 53

Total success

Mean attempts

Complications

44% vs 92%

2.5 vs 1.4

0% vs 0%NS

ICU ED ICU ED + MICU ORs ED PEA arrest

900 130 29 201 160 40

94.4% vs 100% 78.5% vs 93.9% 65% vs 100% 64% vs. 98% 96% vs 100% NS 65% vs 90%

2.6 vs 1.1 3.5 vs 1.6 3.12 vs 1.75 5.2 vs 2.3 2.8 vs 1.4 5.0 vs 2.3

6.7% vs 1.1% 7.7% vs 1.5% NR 13% vs 3% 8.43% vs 1.39%NS 20% vs 0%

ED

122

NR

3.52 vs 1.55

14% vs 12% NS,4

NR

196

98.1% vs 91.2%

NR

9.7% vs 0% 0% vs 0%

ED

40

62.5% vs 81.3%

2.0 vs 2.0NS

OR

284

93.9% vs 99.4%

1.31 vs 1.23NS

4.3% vs 1.8% NS

OR

462

86.2% vs 97.9%

NR

8.1% vs 5.9%NS

ICU

484

NR

NR

9% vs 11%NS, 3

98.7%

NR

0%

Wards Pts ⬎65 y/o

72

P ⬍ 0.05 unless otherwise noted. Abbreviations: RCT= randomized controlled trial; ICU = intensive care unit; ED = emergency department; PEA = pulseless electrical activity; NR = not reported; NS, not significant. 3 Alternating days. 4 Including hematoma. 5 Based on operator availability.

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Chapter 12 – Ultrasound Guidance of Vascular Catheterization

Table 12.3.

Studies of dynamic ultrasound use in pediatric populations

First author/Year

Study type

Patient population

n

Total success

Mean attempts

Complications6

Verghese 200050 Leyvi 200451

RCT Retrospective

Pts ⬍10 kg for OHS Peds pts for OHS

45 149

81% vs 94% 72.5% vs 91.5%

2 vs 17 NR

19% vs 6% 4.9% vs 6.4%

Abbreviations: RCT = randomized controlled trial; LM = landmark; pts, patients; OHS = open heart surgery; NR = not reported; Peds = pediatrics. 6 Major complications unless otherwise noted (arterial puncture, pneumothorax, hemothorax). 7 Study-reported medians.

To date, three major meta-analyses have been published, each of which confirmed these findings. Randolph and colleagues18 reviewed the eight randomized controlled trials available at the time, finding that ultrasound use significantly decreased the risk of failed catheter placement regardless of site of insertion (RR 0.32, 95% CI 0.18–0.55), reduced mechanical complications of placement (RR 0.22, 95% CI 0.10–0.45), and reduced the number of attempts required for successful cannulation (RR 0.60, 95% CI 0.45–0.79), although there was no significant change in the time to successful placement (95% CI 80.1–62.2 sec). Of note, the authors did not distinguish between studies using audio Doppler, static ultrasound, and dynamic ultrasound. However, as noted earlier, subsequent data suggest that restriction to dynamic ultrasound would only be expected to increase the magnitude of the observed benefit. Additionally, the analysis included studies with varied definitions of failure, potentially clouding their conclusions. Keenan19 evaluated eighteen randomized controlled trials, including a total of 2092 patients. The analysis differentiated dynamic ultrasound from Doppler and included studies comparing both to landmark techniques. Once again, this metaanalysis confirmed that dynamic ultrasound use reduced the risk of failure (RR 0.40), number of attempts (absolute risk reduction 1.41), and arterial punctures (RR 0.299) when compared with landmark techniques. The study also concluded that dynamic ultrasound was superior to Doppler in all major parameters studied. Again, the studies included had variable definitions of what constituted failed placement, potentially confounding their analysis. Most recently, in a study commissioned by the British National Institute for Clinical Excellence (NICE), Hind and associates20 reviewed the 18 randomized controlled trials of dynamic ultrasound available in 2003, including a total of 1646 patients. This meta-analysis differentiated among technique (dynamic ultrasound vs Doppler), patient population (adult Table 12.4. Traditionally high-risk patient populations in which dynamic ultrasound use has been demonstrated to be safe and effective Significant coagulopathy52 Hematology/oncology patients53 Anatomic contraindications to LM insertion (venous stenosis, extremely low CVP, etc.)54 History of difficult or failed cannulation55 49 Geriatric patients 47 Pulseless patients undergoing CPR Unable to tolerate Trendelenburg positioning56

vs pediatric), and insertion site (IJ, subclavian, or femoral). As expected, this study confirmed that dynamic ultrasound use reduces failure rates of IJ cannulation in pediatric patients (RR 0.15, 95% CI 0.03–0.64) and adult patients (RR 0.14, 95% CI 0.06–0.33), and reiterated the limited data that support dynamic ultrasound over landmark in subclavian and femoral cannulation. In addition to being superior for patient-related outcomes, dynamic ultrasound may be cost-effective from an economic standpoint. However, limited studies exist to support this claim. Calvert and coworkers21 analyzed data from 20 randomized controlled trials and confirmed the superiority of dynamic ultrasound over landmark techniques. They went on to calculate the cost-effectiveness of dynamic ultrasound use, including initial equipment costs, training costs, and maintenance costs in their analysis as compared with the cost of complications and delayed cannulation. Based on conservative estimates, the authors calculate that for every 1000 CVC placements, dynamic ultrasound use would save approximately £2000 (about $4000 in 2008).

Future directions Significant data support the superiority of dynamic ultrasound in terms of patient outcomes, and some data suggest costeffectiveness. However, there is limited evidence of the level of training or operator experience required to achieve optimal outcomes using ultrasound guidance. The majority of studies cited previously included a one- to six-hour training period on ultrasound use prior to randomization to the ultrasound wing of the study. In comparison with historical data on landmark CVC placement, which suggested that up to 50 procedures were necessary to obtain optimal results, some authors have suggested that because of the rapid learning curve observed anecdotally for ultrasound-guided CVC placement, four hours of training in general ultrasound and its application to CVC placement, and only five to ten proctored examinations, are sufficient for competence.22 However, this assertion has yet to be validated. Several models, including cadaveric models23 and inexpensive homemade systems using materials such as gelatin and latex tubing,24,25 are described in the literature to facilitate training in ultrasound techniques. Use of these models increases ultrasound use by participants, presumably because of increased familiarity of the technique, but quality outcome data are lacking.

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Despite the data supporting its use, several surveys conducted as recently as 2007 have demonstrated that implementation of dynamic ultrasound for CVC placement remains limited, with between 11 percent and 20 percent of respondents using ultrasound most of the time.26–29 The most significant barriers to implementation were the availability of adequate ultrasound equipment and perceived usefulness of dynamic ultrasound among respondents. However, three of the four published surveys were conducted in Britain, and may not reflect current trends in the United States. Further studies aimed at identifying and overcoming specific barriers to ultrasound use are needed to facilitate its widespread implementation. Additionally, and of note, to our knowledge no study at this time has demonstrated that ultrasound use significantly alters rates of CVC infection or catheter sepsis, nor has it been demonstrated to reduce ICU length of stay or overall patient morbidity or mortality parameters. If these analyses are conducted and prove to be favorable, they may encourage use of ultrasound and decrease barriers to its implementation. Several recent studies have expanded the traditional role of dynamic ultrasound as a guide for initial puncture of the target vein. These studies suggest that, as practitioners become more comfortable with ultrasound use, dynamic ultrasound may be used effectively to confirm correct guidewire placement within the vein during the cannulation procedure30,31 and to rapidly detect the presence of a pneumothorax after the procedure before portable chest X-ray is possible.32 However, additional studies confirming the reproducibility and reliability of these techniques are needed before use becomes widespread.

Credentialing In preparation of this chapter, an informal survey of several anesthesiology departments revealed that not a single one required separate credentialing for use of ultrasound to assist in CVC insertion. However, the American Medical Association states that ultrasound imaging privileging should be specifically delineated by department based on background and training, although this recommendation may have been written without the specific consideration of the very narrow scope of ultrasound for vascular access. Various professional societies have mandated incorporation of ultrasound training in their residency programs, most notably the American College of Emergency Physicians and the American College of Surgeons, but again, the narrow scope of ultrasound solely for vascular access is not the main intent of this mandated training. Given that ultrasound does require skill acquisition and that incorrect use (e.g. failure to distinguish right from left, recognize intravascular thrombus) can be associated with an increase in morbidity, we recommend that basic documented training and credentialing should become standard. Given that training and credentialing of central line insertion are already ubiquitous, perhaps simply adding ultrasound use for this procedure in the training and credentialing process makes the most sense. This will be more important if the technique is adopted

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widely as the standard of care, or even if there is only agreement that, at least, it should always be available.

Practice parameters Compelling data from numerous randomized controlled trials and multiple meta-analyses support the superiority of dynamic ultrasound use for CVC placement when compared with landmark techniques. Both intuitively and from the literature, there are a variety of situations in which landmark techniques place the patient at particularly high risk for failure and mechanical complication. In these high-risk scenarios, we feel strongly that ultrasound guidance should be considered the standard of care. One such situation is a known or anticipated lack of traditional landmarks such as in morbid obesity, prior neck surgery or radiation, or cannulation of sites such as the deep brachial vein, which lack definite anatomic landmarks. Other scenarios in which we feel strongly that dynamic ultrasound guidance represents standard of care are (1) patients who have had multiple prior access procedures (e.g. hematology/oncology patients), because the vein might be thrombosed or stenosed; (2) patients who should be put at the lowest risk of a carotid puncture (e.g. prior vascular intervention or known large plaque); and (3) patients who are at higher than usual risk of complication from vascular mishap (e.g. anticoagulated or thrombocytopenic patients). Based on the data discussed earlier, governmental organizations have recognized the potential benefit of ultrasound guidance. In 2002, NICE recommended that this be made the standard of care, stating, “Two-dimensional (2-D) imaging ultrasound guidance is recommended as the preferred method for insertion of central venous catheters (CVCs) into the internal jugular vein (IJV) in adults and children in elective situations. The use of two-dimensional (2-D) imaging ultrasound guidance should be considered in most clinical circumstances where CVC insertion is necessary either electively or in an emergency situation.”33 This recommendation was reviewed, updated, and confirmed in 2005. In the United States, the Agency for Healthcare Research and Quality (AHRQ) recommended in 2001 that ultrasound guidance be one of eleven procedures that “were rated most highly in terms of strength of the evidence supporting more widespread implementation.”34 Despite the existing evidence and governmental recommendations, it remains controversial whether use of ultrasound guidance should be considered standard of care in all situations, and, as discussed earlier, multiple barriers exist to its widespread adoption. Many anesthesiologists and hospitals do not have ultrasound devices at their disposal, are not adequately trained or do not routinely employ these devices, and/or have not recognized similar improvements in procedural outcome as demonstrated in the published literature. Benefits of ultrasound guidance may not be realized until operators who are comfortable with traditional techniques gain experience and comfort with ultrasound guidance. Furthermore, the meta-analyses that have been published to date are limited by the data available at

Chapter 12 – Ultrasound Guidance of Vascular Catheterization

the time of analysis, and because of the rapid evolution of ultrasound availability and use, may no longer be applicable. At the time of writing, there is an active Cochrane review that will attempt to determine more definitively the efficacy and generalizability of ultrasound guidance for central venous cannulation. We expect this study to confirm what has been previously demonstrated in randomized controlled trials and metaanalyses, which will facilitate a more widespread adoption of ultrasound use in central line placement.35

References

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19. 1. Troianos CA, Kuwik R, Pasqual P, et al. Internal jugular vein and carotid artery anatomic relation as determined by ultrasound. Anesthesiology 1996;85:43–48. 2. Maecken T, Grau T. Ultrasound imaging in vascular access. Crit Care Med 2007;35:S178–85. 3. Eisen L, Narasimhan M, Berger J, et al. Mechanical complications of central venous catheters. J Intensive Care Med 2006;21:40–46. 4. Merrer J, De Jonghe B, Golliot F, et al. Complications of femoral and subclavian venous catheterization in critically ill patients: A randomized controlled trial. JAMA 2001;286:700–7. 5. Mansfield P, Hohn D, Fornage B, et al. Complications and failures of subclavian-vein catheterization. N Engl J Med 1994; 331:1735–8. 6. Sznajder J, Zveibil F, Bitterman H, et al. Central vein catheterization: failure and complication rates by three percutaneous approaches. Arch Intern Med 1986;146:259–61. 7. Johnson E, Saltzman D, Suh G, et al. Complications and risks of central venous catheter placement in children. Surgery 1998;124:911–6. 8. Casado-Flores J, Barja J, Martino R, et al. Complications of central venous catheterization in critically ill children. Pediatr Crit Care Med 2001;2:57–62. 9. Bernard RW, Stahl WM. Subclavian vein catheterizations: a prospective study. I. Noninfectious complications. Ann Surg 1971;173:184–90. 10. Bold RJ, Winchester DJ, Madary AR, Gregurich MA, Mansfield PF. Prospective, randomized trial of Doppler-assisted subclavian vein catheterization. Arch Surg 1998;133:1089–93. 11. Gilbert TB, Seneff MG, Becker RB. Facilitation of internal jugular venous cannulation using an audio-guided Doppler ultrasound vascular access device: results from a prospective, dual-center, randomized, crossover clinical study. Crit Care Med 1995;23:60–65. 12. Verghese ST, McGill WA, Patel RI, Sell JE, Midgley FM, Ruttimann UE. Comparison of three techniques for internal jugular vein cannulation in infants. Paediatr Anaesth 2000;10:505–11. 13. Arai T, Yamashita M. Central venous catheterization in infants and children – small-caliber audio-Doppler probe versus ultrasound scanner. Paediatr Anaesth 2005;15:858–61. 14. Chuan WX, Wei W, Yu L. A randomized-controlled study of ultrasound prelocation vs anatomical landmark-guided cannulation of the internal jugular vein in infants and children. Paediatr Anaesth 2005;15:733–8. 15. Milling TJ Jr, Rose J, Briggs WM, et al. Randomized, controlled clinical trial of point-of-care limited ultrasonography assistance of central venous cannulation: the Third Sonography Outcomes

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Assessment Program (SOAP-3) Trial. Crit Care Med 2005;33:1764–9. Hosokawa K, Shime N, Kato Y, Hashimoto S. A randomized trial of ultrasound image-based skin surface marking versus real-time ultrasound-guided internal jugular vein catheterization in infants. Anesthesiology 2007;107:720–4. Hayashi H, Amano M. Does ultrasound imaging before puncture facilitate internal jugular vein cannulation? Prospective randomized comparison with landmark-guided puncture in ventilated patients. J Cardiothorac Vasc Anesth 2002;16: 572–5. Randolph AG, Cook DJ, Gonzales CA, Pribble CG. Ultrasound guidance for placement of central venous catheters: a meta-analysis of the literature. Crit Care Med 1996;24:2053–8. Keenan SP. Use of ultrasound to place central lines. J Crit Care 2002;17:126–37. Hind D, Calvert N, McWilliams R, et al. Ultrasonic locating devices for central venous cannulation: meta-analysis. BMJ 2003;16:327–61. Calvert N, Hind D, McWilliams RG, Thomas SM, Beverley C, Davidson A. The effectiveness and cost-effectiveness of ultrasound locating devices for central venous access: a systematic review and economic evaluation. Health Technol Assess 2003;7:1–84. Feller-Kopman D. Ultrasound-guided internal jugular access: a proposed standardized approach and implications for training and practice. Chest 2007;132:302–9. Nip IL, Haruno MM. A systematic approach to teaching insertion of a central venous line. Acad Med 2000;75:552. Di Domenico S, Santori G, Porcile E, Licausi M, Centanaro M, Valente U. Inexpensive homemade models for ultrasound-guided vein cannulation training. J Clin Anesth 2007;19:491–6. Kendall JL, Faragher JP. Ultrasound-guided central venous access: a homemade phantom for simulation. CJEM 2007;9: 371–3. Bailey PL, Glance LG, Eaton MP, Parshall B, McIntosh S. A survey of the use of ultrasound during central venous catheterization. Anesth Analg 2007;104:491–7. Tovey G, Stokes M. A survey of the use of 2D ultrasound guidance for insertion of central venous catheters by UK consultant paediatric anaesthetists. Eur J Anaesthesiol 2007;24:71–5. Girard TD, Schectman JM. Ultrasound guidance during central venous catheterization: a survey of use by house staff physicians. J Crit Care 2005;20:224–9. Jefferson P, Ogbue MN, Hamilton KE, Ball DR. A survey of the use of portable ultrasound for central vein cannulation on critical care units in the UK. Anaesthesia 2002;57:365–8. Stone MB. Identification and correction of guide wire malposition during internal jugular cannulation with ultrasound. CJEM 2007;9:131–2. Howes B, Dell R. Ultrasound to detect incorrect guidewire positioning during subclavian line insertion. Anaesthesia 2006;61:615 Maury E, Guglielminotti J, Alzieu M, Guidet B, Offenstadt G. Ultrasonic examination: an alternative to chest radiography after central venous catheter insertion? Am J Respir Crit Care Med 2001;164:403–5. National Institute for Clinical Excellence. Guidance on the Use of Ultrasound Locating Devices for Placing Central Venous Catheters. London: National Institute for Clinical Excellence, September 2002, reviewed August 2005. Available online at http://www.nice. org.uk/nicemedia/pdf/Ultrasound 49 GUIDANCE.pdf.

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34. Rothschild, JM. Ultrasound guidance of central vein catheterization. In Making Health Care Safer: A Critical Analysis of Patient Safety Practices. Evidence Report/Technology Assessment, No. 43. AHRQ Publication No. 01-E058, July 2001. Rockville, MD: Agency for Healthcare Research and Quality, http://www.ahrq.gov/clinic/ptsafety. 35. Brass P, Hellmich M, Kolodziej, L, et al. Traditional landmark versus ultrasound guidance for central vein catheterization. Cochrane Database Syst Rev 1: CD0069262, 2008. 36. Gualtieri E, Deppe SA, Sipperly ME, Thompson DR. Subclavian venous catheterization: greater success rate for less experienced operators using ultrasound guidance. Crit Care Med 1995;23:692–7. 37. Karakitsos D, Labropoulos N, De Groot E, et al. Real-time ultrasound-guided catheterisation of the internal jugular vein: a prospective comparison with the landmark technique in critical care patients. Crit Care 2006;10:R162. 38. Leung J, Duffy M, Finckh A. Real-time ultrasonographically guided internal jugular vein catheterization in the emergency department increases success rates and reduces complications: a randomized, prospective study. Ann Emerg Med 2006;48: 540–7. 39. Mallory DL, McGee WT, Shawker TH, et al. Ultrasound guidance improves the success rate of internal jugular vein cannulation. A prospective, randomized trial. Chest 1990;98:157–60. 40. Milling T, Holden C, Melniker L, Briggs WM, Birkhahn R, Gaeta T. Randomized controlled trial of single-operator vs. two-operator ultrasound guidance for internal jugular central venous cannulation. Acad Emerg Med 2006;13: 245–7. 41. Troianos CA, Jobes DR, Ellison N. Ultrasound-guided cannulation of the internal jugular vein. A prospective, randomized study. Anesth Analg 1991;72:823–6. 42. Hilty WM, Hudson PA, Levitt MA, Hall JB. Real-time ultrasound-guided femoral vein catheterization during cardiopulmonary resuscitation. Ann Emerg Med 1997;29: 331–6. 43. Miller AH, Roth BA, Mills TJ, Woody JR, Longmoor CE, Foster B. Ultrasound guidance versus the landmark technique for the placement of central venous catheters in the emergency department. Acad Emerg Med 2002;9:800–5. 44. Cajozzo M, Quintini G, Cocchiera G, et al. Comparison of central venous catheterization with and without ultrasound guide. Transfus Apher Sci 2004;31:199–202.

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45. Hrics P, Wilber S, Blanda MP, Gallo U. Ultrasound-assisted internal jugular vein catheterization in the ED. Am J Emerg Med 1998;16:401–3. 46. Wigmore TJ, Smythe JF, Hacking MB, Raobaikady R, MacCallum NS. Effect of the implementation of NICE guidelines for ultrasound guidance on the complication rates associated with central venous catheter placement in patients presenting for routine surgery in a tertiary referral centre. Br J Anaesth 2007;99(5):662–5. 47. Augoustides JG, Diaz D, Weiner J, Clarke C, Jobes DR. Current practice of internal jugular venous cannulation in a university anesthesia department: influence of operator experience on success of cannulation and arterial injury. Cardiothorac Vasc Anesth 2002;16:567–71. 48. Martin MJ, Husain FA, Piesman M, et al. Is routine ultrasound guidance for central line placement beneficial? A prospective analysis. Curr Surg 2004;61:71–4. 49. Cajozzo M, Cocchiara G, Greco G, et al. Ultrasound (US) guided central venous catheterization of internal jugular vein on over 65-year-old patients versus blind technique. J Surg Oncol 2004;88:267–8. 50. Verghese ST, McGill WA, Patel RI, Sell JE, Midgley FM, Ruttimann UE. Ultrasound-guided internal jugular venous cannulation in infants: a prospective comparison with the traditional palpation method. Anesthesiology 1999;91:71–7. 51. Leyvi G, Taylor DG, Reith E, Wasnick JD. Utility of ultrasound-guided central venous cannulation in pediatric surgical patients: a clinical series. Paediatr Anaesth 2005;15:953–8. 52. Tercan F, Ozkan U, Oguzkurt L. US-guided placement of central vein catheters in patients with disorders of hemostasis. Eur J Radiol 2008;65:253–6. 53. Mey U, Glasmacher A, Hahn C, et al. Evaluation of an ultrasound-guided technique for central venous access via the internal jugular vein in 493 patients. Support Care Cancer 2003;11:148–55. 54. Fry WR, Clagett GC, O’Rourke PT. Ultrasound-guided central venous access. Arch Surg 1999;134:738–40. 55. Hatfield A, Bodenham A. Portable ultrasound for difficult central venous access. Br J Anaesth 1999;82:822–6. 56. Schummer W, Schummer C, Tuppatsch H, Fuchs J, Bloos F, H¨uttemann E. Ultrasound-guided central venous cannulation: is there a difference between Doppler and B-mode ultrasound? J Clin Anesth 2006;18:167–72.

Chapter

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Ultrasound guidance for regional anesthesia procedures Christina L. Jeng and Meg A. Rosenblatt

Introduction Peripheral nerve blocks have traditionally been performed employing anatomic landmarks to locate sensory and motor nerves. Over the past two decades, nerve stimulation (NS) techniques have increased in popularity, using concentrated electrical impulses to depolarize, stimulate, and thus identify specific nerves. In recent years, the application of ultrasound (US) to visualize nerves and the spread of local anesthetic has revolutionized the practice of regional anesthesia. US-guided regional anesthesia requires knowledge of the anatomy as well as basic ultrasound principles, which will allow practitioners to choose their equipment wisely. A number of linear and curved array US probes are available, and newer echogenic needles with distance markers continue to improve visualization. Portable US machines are available that will provide diagnostic-quality images for block performance. Generally, linear array probes provide excellent near-field visualization. The higher-frequency ultrasound waves provide the best image resolution but are limited by depth penetration. Greater penetration requires lower-frequency ultrasound waves; however, these lower frequencies result in poorer image resolution. For superficial targets, including most peripheral nerves, the high-frequency linear array US probes are sufficient; they provide excellent near-field visualization with high resolution. US imaging for upper extremity blocks is straightforward, because the brachial plexus and peripheral nerves are superficial (within centimeters of the skin) even in patients with high body mass indexes (Figures 13.1, 13.2). For these blocks, a linear array 38-mm high-frequency (10–15 MHz) US probe is ideal, and a smaller probe (25 mm) should be considered for most upper extremity blocks secondary to the limited anatomic space. For deeper structures, such as the the infraclavicular region, a lower-frequency probe (≤7 MHz) may be necessary to obtain better ultrasound penetration. Imaging of nerves in the lower extremities can be more challenging because the target structures are deeper within muscle and adipose tissue (Figure 13.3). For these blocks, a phased array lower-frequency (5–7 MHz) probe will provide greater penetration and is necessary to scan a wider anatomic area, thus facilitating imaging.1 Therefore, the probes chosen should have the highest possible frequency and still allow adequate tissue penetration for imaging of the target nerve and surrounding structures.2

Needle visualization may be optimized by minimizing refraction and maximizing reflection. This is accomplished by maintaining the needle perpendicular to the US beam. There are two options available for needle visualization: in-plane and out-of-plane techniques. With the in-plane technique, the needle is advanced in-line and parallel to the transducer. Both the needle and the shaft of the needle may be visualized within the entire US sector. In the out-of-plane technique, the needle is placed perpendicular to the transducer. The needle is visualized as a single point in the US image. For deeper targets, the out-of-plane technique is preferable. For more superficial nerve targets, the in-plane technique is preferred because the entire needle may be visualized as it approaches its target.2 Needle choice for optimal US image is controversial. Echogenic, insulated, B-bevel needles are most commonly used for peripheral nerve blocks. Klein and colleagues describe the use of a piezoelectric vibrating needle and catheter for enhancing the US image and confirming the location of the needle or catheter tip.3 Using a synthetic phantom, Deam and associates improved visibility under ultrasound with echogenic “textured” needles.4 After investigating 12 needles, Maecken and coworkers concluded that there is yet no ideal choice and that the improvement of needles for use under US guidance is necessary.5

Evidence of utility Ultrasound has allowed practitioners to determine the sensitivity of traditional localization techniques. Perlas and associates studied 103 patients who were undergoing forearm or hand surgery.6 During the performance of an US-guided axillary

MSM

ASM

Figure 13.1. Anatomy of the interscalene groove. ASM: anterior scalenus muscle, MSM: middle scalenus muscle; arrows: nerves within interscalene groove.

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SCA Lat

Med

Figure 13.2. Anatomy requisite for the performance of a supraclavicular block. SCA: subclavian artery. Arrows identify the nerves of the brachial plexus at the level of the divisions, lateral to the artery.

block, a 22-gauge insulated needle was placed in direct contact with one of the nerve branches. A paresthesia perceived by the patients and then a motor response to nerve stimulation at 0.5 mA were sought. Paresthesia was 38 percent sensitive and motor response 74.5 percent sensitive for needle nerve contact. To elicit a paresthesia, the needle must be in contact with a sensory nerve, just as a motor response requires contact with a motor nerve. Urmey and colleagues and Bollini and coworkers were unable to correlate the elicitation of a sensory paresthesia to the ability to elicit a motor response with peripheral nerve stimulation in immobile needles while performing interscalene blocks.7,8 Neither paresthesia nor NS are reliable techniques for the performance of neuronal blockade.

Figure 13.3. Sciatic nerve at the subgluteal level. Note the depth marker at 4.3 cm.

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For both upper and lower extremity blocks, US decreases the time to successful placement, improves quality, and increases the duration of blocks. Comparing 56 patients who were undergoing elective hand surgery under either transarterial axillary (TA) or US-guided perivascular block, Sites and colleagues found that whereas eight of the patients (28%) in the TA group required conversion to general anesthesia, none in the US group did.9 The time needed to perform the block using the US technique was also significantly shorter (7.9 ± 3.9 min vs 11.1 ± 5.7 min, P = 0.05). Not only did Williams and associates demonstrate a significant decrease in the execution time to perform supraclavicular blocks when US is added to a NS technique (5.0 min vs 9.8 min, P = 0.0001), but they also found that the quality of the block, particularly of the ulnar nerve distribution, was significantly improved with the use of US.10 When comparing an US group with a NS group for interscalene block, Kapral and associates demonstrated that surgical anesthesia (sensory, motor, and extent of blockade) was significantly better in the US group (99% vs 91%, P ⬍ 0.01).11 For lower-extremity blocks, Marhofer and colleagues showed that US guidance improved the quality of sensory block and the onset time of three-in-one blocks in patients undergoing hip surgery after trauma.12 Perlas and coworkers found a statistically significantly higher block success rate when US was used to place sciatic nerve blocks in the popliteal fossa than when NS was employed (89.2% vs 60.6%, P = 0.005).13 The addition of NS does not appear to increase the effectiveness of US techniques. One hundred eighty patients undergoing elective hand surgery were randomized to receive an axillary block performed one of three ways, using (1) three motor response endpoints elicited with NS, (2) real-time in-plane US visualization of the injection of local anesthetic around the three nerves, or (3) nerve stimulation to confirm the US localization of the nerves and readjusting the needles to ensure that stimulation was achieved at 0.5 mA prior to injecting. Block success was higher in the US and US–NS groups (82.9% and 80.7%) than in the NS-alone group (62.9%), but the difference between the US and US–NS groups was not statistically significant.14 The role of nerve stimulation as an adjunct may be limited. Evaluation of 94 consecutive patients for surgery below the elbow under supraclavicular block demonstrated that for adequately US-imaged blocks, confirmation with motor response at less than 0.5 mA did not increase the success rate of the block.15 The use of US may allow successful peripheral nerve block placement in patients in whom traditional methods of nerve localization are limited. Van Geffen and colleagues described several cases of successful neuronal block placement in patients with extensive previous surgery in the region of the planned blocks or demylinating polyneuropathy.16 Blocks were performed for surgical anesthesia and/or postoperative analgesia only with the use of US guidance. In addition, US-guided blocks for surgical anesthesia have been made possible for patients with abnormal coagulation. Khelemsky and associates reported a supraclavicular block in a patient anticoagulated with the

Chapter 13 – Ultrasound Guidance for Regional Anesthesia Procedures

direct thrombin inhibitor argatroban, and Bigeleisen described an infraclavicular brachial plexus block in a patient on a heparin infusion.17,18 In an editorial in the journal Anesthesiology, Hebl discussed the possibility that US-guided regional anesthesia might prevent neurologic injury.19 He speculated that although there will be no effect on surgical risk factors (intraoperative trauma or stretch, vascular compromise, hematoma formation, tourniquet ischemia, or improperly applied immobilizers or casts) or on patient risk factors (male sex, increasing age, preexisting neurologic deficit), the use of US may be able to decrease the anesthesia risk factors of mechanical trauma and local anesthesia toxicity. In fact, the use of US guidance has been shown to provide a 42 percent reduction (P = 0.002) in the volume of ropivacaine required to block the femoral nerve compared with the use of NS to perform the same block.20 Two recent case reports of accidental intravascular injection of local anesthetic resulting in seizures after properly performed US guided blocks, though, have highlighted the need to continually employ safe techniques, including slow injection of small aliquots with aspiration between them, even when blocks are performed under US visualization.21,22 The use of ultrasound has enabled regionalists to diagnose nonneural pathology. Sites and colleagues reported three cases in which vascular lesions – clots in the femoral vein, femoral artery, and carotid artery – were diagnosed on scanning to perform anesthetic blocks, and ultimately resulted in therapeutic and anesthetic management changes.23

Complications There are multiple reports of upper-extremity musculoskeletal and back disorders as occupational hazards among ultrasonographers. In a pilot survey of 340 diagnostic medical sonographers, one-third of the responders reported at least one workrelated symptom in the upper extremity – most frequently, paresthesia and numbness or finger pain. Carpal tunnel syndrome was diagnosed in 1.5 percent of cases, and more than 60 percent of sonographers experienced neck and low back pain.24 Schoenfeld and colleagues described “transducer user syndrome” among sonographers in obstetrics and gynecology, which included carpal tunnel syndrome, carpal instability, tendonitis, weakness, motion restriction, and back, shoulder, or neck pain.25 These same symptoms have also been reported among cardiac sonographers.26 It is possible that these types of complications could be expected for regionalists using US in busy practices. US causes tissue injury by thermal and nonthermal mechanisms. Because normal variations in core temperature of several degrees Celsius occur naturally, the temperature increase secondary to US exposure for short periods of time has no significant biological effects.27 Unlike other imaging modalities, diagnostic US induces mechanical strain on tissues, especially those containing dissolved gas. However, any damage heals quickly and completely with no clinically significant effect. In tissues

not containing gas, there is no evidence of adverse effect. Acceleration of bone healing and auditory or tactile sensation may also occur. None of these effects poses a risk to the health of the patient.28

Credentialing Learning US-guided regional anesthesia is challenging. It requires an intimate knowledge of anatomy as well as the ability to interpret ultrasound images. The operator must be able to use each hand independently while continuously looking at the screen. Sites and associates studied the learning curve associated with a simulated US-guided interventional task by inexperienced anesthesia residents.29 Using US guidance, the residents were asked to place a 22-gauge B-bevel needle into an olive buried inside a turkey breast. Upon successive trials, the time for each subject to perform the task was reduced and accuracy improved. However, this trial also identified a “concerning novice pattern” in which subjects advanced the needle without adequate visualization, resulting in excessive depth of penetration of the needle. The researchers then studied six anesthesia residents on a dedicated one-month US-regional anesthesia rotation as the residents performed a total of 520 nerve blocks.30 Again, speed and accuracy improved throughout the rotation, but five “quality-compromising patterns of behavior” were identified: (1) failure to recognize maldistribution of local anesthesia, (2) failure to recognize inappropriate needle tip location, (3) operator fatigue, (4) incorrectly correlating sidedness of patient with sidedness of US image, and (5) poor choice of needle-insertion site and angle, resulting in difficult or absent needle visualization. Although errors continued to occur, they seemed to reach a consistent nadir after approximately 71 to 80 blocks were performed. Is credentialing necessary to use US for procedures that have been for years performed blindly? Is not any visualization likely to be an improvement or be potentially safer than traditional techniques? In response to the World Health Organization’s recommendations, in its report on training in diagnostic US, that professional associations should be actively involved in developing training programs,31 the American Society of Regional Anesthesia (ASRA) has taken a leadership role in providing lectures and workshops at its annual meetings. Currently the ASRA, in association with the European Society of Regional Anesthesia (ESRA), has recommended guidelines for education and training in US-guided regional anesthesia. The ASRA and ESRA have defined a list of 10 common skills that should be acquired during US training. They appear in Table 13.1. Proficiency in US-guided regional anesthesia can be divided into four major categories, each with a defined skill set. The first skill set involves understanding US image generation and operation – basic principles of image generation, selection of appropriate transducer, depth and focus settings, use of time gain compensation and overall gain, use and application of color Doppler, and orientation of screen to patient. Image

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Table 13.1. 1. 2. 3. 4. 5. 6. 7. 8. 9. 10.

ASRA– ESRA recommended skills

Ability to visualize key landmark structures (i.e. blood vessels, muscles, fascia, and bone) Identification of nerves/plexus on short axis imaging Confirmation of normal anatomy and recognizing anatomic variations Plans for needle approach avoiding unnecessary tissue trauma Maintenance of aseptic technique Ability to follow needle to target in real time Consideration of confirmation of proper needle placement (e.g. nerve stimulation) Test injection of local anesthetic and visualization Proper needle adjustment to visualize appropriate local anesthetic spread through entirety of injection Maintenance of traditional safety guidelines (i.e. immediate availability of resuscitation equipment, standard monitoring, frequent aspiration for blood to avoid intravascular injection, and acknowledgment of patient response)

Source: Sites BD, Chan VW, Neal JM, et al. The American Society of Regional Anesthesia and Pain Medicine and the European Society of Regional Anaesthesia and Pain Therapy Joint Committee Recommendations for Education and Training in Ultrasound-Guided Regional Anesthesia. Reg Anesth Pain Med 2009;34:40–6.

optimization (not related to the US device) and image interpretation constitute the second and third skill sets. Image optimization includes learning to apply appropriate transducer pressure, alignment, rotation, and tilting. Image interpretation incorporates the ability to identify nerves, muscles and fascia, blood vessels (distinguishing artery from vein), bone, and pleura, as well as common acoustic and anatomic artifacts. The final set of skills important in determining proficiency consists of proper needle insertion and injection of local anesthetic. In-plane and out-of-plane techniques should be mastered, and the benefits and limitations of each technique should be recognized. Familiarity with correct local anesthetic spread, minimization of unintentional transducer movement, proper ergonomics, and ability to identify intraneural needle location are all skills within this category.32 There are still no specific recommendations for credentialing of individual practitioners to perform US-guided regional anesthesia; however, each institution should have its own individualized credentialing process.

Conclusions The application of US to the practice of regional anesthesia has not only advanced our knowledge but has also decreased the time to perform blocks, increased their success, allowed the provision of blocks for those who may not otherwise be candidates, and may ultimately prove to improve safety. Hopkins hopes that the use of US will not be “paralyzed by an inability to satisfy the lust for the highest levels of evidence-based medicine,” because this technology is such a significant “stepchange” in the way regional anesthesia is practiced.33 With appropriate training and experience, US-guided regional anesthesia has proved itself a safe and effective technology.

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References 1. Marhofer P, Chan VW. Ultrasound-guided regional anesthesia: current concepts and future trends. Anesth Analg 2007; 104:1265–9. 2. Sites BD, Brull R, Chan VW, et al. Artifacts and pitfall errors associated with ultrasound-guided regional anesthesia. Part I: understanding the basic principles of ultrasound physics and machine operations. Reg Anesth Pain Med 2007;32: 412–8. 3. Klein SM, Fronheiser MP, Reach J, Nielsen KC, Smith SW. Piezoelectric vibrating needle and catheter for enhancing ultrasound-guided peripheral nerve blocks. Anesth Analg 2007;105:1858–60. 4. Deam RK, Kluger R, Barrington MJ, McCutcheon CA. Investigation of a new echogenic needle for use with ultrasound peripheral nerve blocks. Anaesth Intensive Care 2007;35:582–6. 5. Maecken T, Zenz M, Grau T. Ultrasound characteristics of needles for regional anesthesia. Reg Anesth Pain Med 2007;32:440–7. 6. Perlas A, Niazi A, McCartney C, et al. The sensitivity of motor response to nerve stimulation and paresthesia for nerve localization as evaluated by ultrasound. Reg Anesth Pain Med 2006;31:445–50. 7. Urmey WF, Stanton S. Inability to consistently elicit a motor response following sensory paresthesia during interscalene block administration. Anesthesiology 2002;96:552–4. 8. Bollini CA, Urmey WF, Vascello L, Cacheiro F. Relationship between evoked motor response and sensory paresthesia in interscalene brachial plexus block. Reg Anesth Pain Med 2003;28(5):384–8. 9. Sites BD, Beach ML, Spence BC, Wiley CW, Hartman GS Gallagher JD. Ultrasound guidance improves the success rate of perivascular axillary plexus block. Acta Anaesthesiol Scand 2006;50:687–84. 10. Williams SR, Chouinard P, Arcand G, et al. Ultrasound guidance speeds execution and improves the quality of supraclavicular block. Anesth Analg 3003;97:1518–23. 11. Kapral S, Greher M, Huber G, et al. Ultrasonographic guidance improves the success rate of interscalene brachial plexus blockade. Reg Anesth Pain Med 2008;33(3):253–8. 12. Marhofer P, Schrogendorfer K, Konig H, et al. Ultrasonographic guidance improves sensory block and onset time of three-in-one blocks. Anest Analg 1997;85:854–7. 13. Perlas A, Brull R, Chan VWS, et al. Ultrasound guidance improves the success of sciatic nerve block at the popliteal fossa. Reg Anesth Pain Med 2008;33:259–65. 14. Chan VWS, Perlas A, McCartney CJL, Brull R, Xu D. Ultrasound guidance improves success rate of axillary brachial plexus block. Can J Anesth 2007;54:176–82. 15. Beach ML, Sites BD, Gallagher JD. Use of a nerve stimulator does not improve the efficacy of ultrasound-guided supraclavicular nerve blocks. J Clin Anesth 2006;18:580–4. 16. Van Geffen GJ, McCartney CJL, Gielen M, Chan VWS. Ultrasound as the only nerve localization technique for peripheral nerve block. J Clin Anesth 2007;19:381–5. 17. Khelemsky Y, Rosenblatt MA. Ultrasound-guided supraclavicular block in a patient anticoagulated with argatroban. Pain Pract 2008;8(2):152. 18. Bigeleisen PE. Ultrasound-guided infraclavicular block in an anticoagulated and anesthetized patient. Anesth Analg 2007;104(5):1285–7.

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19. Hebl JR. Ultrasound-guided regional anesthesia and the prevention of neurologic injury: fact or fiction? Anesthesiology 2008;108:186–88. 20. Casati A, Baciarello M, Di Cianni S, et al. Effects of ultrasound guidance on the minimum effective anaesthetic volume required to block the femoral nerve. Br J Anaesth 2007;98:823–7. 21. Loubert C, Williams SR, Helie F, Acand G. Complication during ultrasound-guided regional block: accidental intravascular injection of local anesthetic. Anesthesiology 2008;108:759–60. 22. Zetlaoui PJ, Labbe J, Benhamou D. Ultrasound guidance for axillary plexus block does not prevent intravascular injection. Anesthesiology 2008;108:761. 23. Sites BD, Spence BC, Gallagher JD, Beach ML. On the edge of the ultrasound screen: regional anesthesiologists diagnosing nonneural pathology. Reg Anesth Pain Med 2006;31:555–62. 24. Mirk P, Magnavita N, Masini L, Bazzocchi M, Fileni A. Frequency of musculoskeletal symptoms in diagnostic medical sonographers. Results of a pilot survey. Radiol Med (Torino) 1999;98:236–41. 25. Schoenfeld A, Goverman J, Weiss DM, Meizner I. Transducer user syndrome: an occupational hazard of the ultrasonographer. Eur J Ultrasound 1999;10:41–5. 26. Vanderpool HE, Friis EA, Smith BS, Harms KL. Prevalence of carpal tunnel syndrome and other work-related musculoskeletal problems in cardiac sonographers. J Occup Med 1993;35:604–10.

27. O’Brien WD, Deng CX, Harris GR, et al. The risk of exposure to diagnostic ultrasound in postnatal subjects – thermal effects. J Ultrasound Med 2008;27:517–35. 28. Church CC, Carstensen EL, Nyborg WL, Carson PL, Frizzell LA, Bailey MR. The risk of exposure to diagnostic ultrasound in postnatal subjects – nonthermal mechanisms. J Ultrasound Med 2008;27:565–92. 29. Sites BD, Gallagher JD, Cravero J, Lundberg J, Blike G. The learning curve associated with a simulated ultrasound-guided interventional task by inexperienced anesthesia residents. Reg Anesth Pain Med 2004;29:544–8. 30. Sites BD, Spence BC, Gallagher JD, et al. Characteristic novice behavior associated with learning ultrasound-guided peripheral regional anesthesia. Reg Anesth Pain Med 2007;32:107–15. 31. World Health Organization. Training in diagnostic ultrasound: essentials, principles and standards. WHO Technical Report Series, No. 875, Geneva: World Health Organization, 1998. 32. Sites BD, Chan VW, Neal JM, et al. The American Society of Regional Anesthesia and Pain Medicine and the European Society of Regional Anaesthesia and Pain Therapy Joint Committee Recommendations for Education and Training in Ultrasound-Guided Regional Anesthesia. Reg Anesth Pain Med 2009;34(1):40–6. 33. Hopkins PM. Ultrasound guidance as a gold standard in regional anesthesia. Br J Anaesth 2007;98:299–301.

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Respiratory gas monitoring James B. Eisenkraft

Introduction Gases of interest to the anesthesia caregiver include oxygen, carbon dioxide, nitrous oxide, and the potent inhaled anesthetic agents. Other gases that may be relevant in certain situations are nitrogen, helium, and nitric oxide. Although gas monitors from different manufacturers may appear to offer various options to the user, ultimately, these monitors use one or more of a limited number of technologies to make the analysis and present the data. The monitoring of respired gases has evolved considerably over the past few years. Contemporary systems are reliable and accurate, have rapid response times, and are becoming less expensive as a result of competition among manufacturers. The early gas monitoring systems were large stand-alone units that were usually placed on a shelf on the anesthesia machine (Figure 14.1). Modern technology has facilitated the miniaturization of these monitors so that on some contemporary anesthesia workstations, the analysis is performed in one component module of a modular physiologic monitoring system

(Figure 14.2). This aim of this chapter is to provide a framework for the understanding of the methods whereby respiratory gases are analyzed, as well as clinical applications, limitations, and pertinent standards of care.

Gas sampling systems For a respired gas mixture to be analyzed, either the gas must be brought to the analyzer or the analyzer must be brought to the gas in the airway. A fuel cell oxygen analyzer located in the breathing system by the inspiratory unidirectional valve is one example of bringing the analyzer to the gas in the circuit. Figure 14.3 shows two different mainstream analyzer modules. Gas is not removed from the circuit for analysis elsewhere, so this is termed a nondiverting or mainstream analyzer. Alternatively, the gas to be analyzed can be sampled continuously from the vicinity of the patient’s airway and conducted via fine-bore tubing (Figure 14.4) to the analyzer unit. Such a design is termed a diverting, or sidestream sampling, system because the gas is diverted from the airway for analysis elsewhere.

Figure 14.1. Left: Datex Capnomac Ultima stand-alone multigas analyzer (circa 1991) that uses infrared analysis for CO2 , N2 O, and anesthetic agents, and paramagnetic analysis for O2 . Right: the much smaller GE Compact Airway module (circa 2001), which uses the same technologies to perform the same functions. White arrows indicate water traps.

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A

Figure 14.2. GE Compact Airway Module shown in Figure 14.1, opened to show miniaturization of gas monitoring technology.

Sidestream (diverting) systems Compared with mainstream analyzers, the advantages of the diverting types of analyzers are that because they are remote from the patient, they can be of any size and therefore offer more versatility in terms of monitoring capabilities. The sampled gas is continuously drawn from the breathing circuit via an adapter placed between the circuit and the patient’s airway (the Y-piece in a circle breathing system) and passes through a water trap (see arrows in Figure 14.1) before entering the analyzer. The gas sampling flow rate is usually about 200 mL/min, with a range of 50 to 250 mL/min. Disadvantages include problems with the catheter sampling system, such as clogging with secretions or water, kinking, failure of the sampling pump, slower response time (although usually ⬍3 sec), and artifacts when the gas sampling rate is poorly matched with the patient’s inspiratory and expiratory gas flow rates. Thus, if a diverting system is used with a very small patient (e.g. a neonate) and the gas sampling rate exceeds the patient’s expiratory gas flow rate, spurious readings may result. Similarly, if an uncuffed tracheal tube is used and

B Figure 14.4. (A) Gas sampling tubing and airway adapter for sidestream sampling gas analyzer. (B) NomolineTM gas sampling line that incorporates a water and water vapor removal system (Phasein AB Medical Technologies, Danderyd, Sweden).

there is a leak between the tube and the trachea, the gas sampling pump may draw room air into the tracheal tube and into the analyzer. Ideally, the gas sampling flow rate should be appropriate for the patient and for the breathing circuit used. Thus the sampling flow rate may limit the ability to use low-flow or closedcircuit anesthesia techniques. If the gas sampling rate exceeds the fresh gas inflow rate, negative pressures potentially can be created in the breathing system.1 Once the sampled gas has been analyzed, it should be directed to the waste gas scavenging system or returned to the patient’s breathing system.

Figure 14.3 (A) Mainstream infrared CO2 analyzer (Hewlett-Packard). (B) Mainstream lightweight infrared multi-agent (CO2 , N2 O, anesthetic agent) analyzer (Phasein AB Medical Technologies, Danderyd, Sweden).

A

B

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In multigas analyzers that incorporate paramagnetic oxygen sensors, simultaneous room air sampling (10 mL/min) is required to provide a reference. This air is therefore added (at a rate of 10 mL/min) to the waste gas exiting the monitor and then may be returned to the patient circuit. This might create a problem during closed-circuit anesthesia, because nitrogen (albeit at a rate of about 8 mL/min) would be added to the breathing circuit (see the section on paramagnetic oxygen analyzer).

Mainstream (nondiverting) systems Until recently, all multigas analyzers were of the diverting or sidestream sampling type. The alternative to a diverting system is a mainstream, or nondiverting, system. Other than for monitoring oxygen by fuel cell, mainstream analysis has, until recently, been available only for carbon dioxide, using infrared technology (Figure 14.3A). By miniaturizing components, mainstream multigas analysis is now available, and a mainstream infrared CO2 , N2 O, and anesthetic agent analyzer is being marketed (Figure 14.3B). Although mainstream analyzers overcome the gas sampling problem, they require a special airway adapter and analysis module to be placed in the breathing system by the patient’s airway. From this location, the mainstream carbon dioxide analyzers produce a sharp capnogram in real time but are vulnerable to damage and add dead space. New designs are light in weight (one ounce), have small dead space, and use solid-state technology (Figure 14.3B). Waste gas scavenging is not required with mainstream gas analysis. Carbon dioxide mainstream analyzer modules placed in the airway are subject to interference by water vapor, secretions, and blood. Because condensed water blocks all infrared wavelengths, leaving too little infrared source intensity to make a measurement, the cuvette’s window is heated (usually to 41◦ C) to prevent such condensation and interference.

Gas analysis systems The respiratory tract and the anesthesia delivery system contain respired gases in the form of molecules. These molecules are in constant motion. When the molecules strike the boundaries of their container, they give rise to pressure (defined as force per unit area); the greater the number of gas molecules present, the greater is the pressure exerted for a given temperature. Dalton’s law of partial pressures states that the total pressure exerted by a mixture of gases is equal to the arithmetic sum of the partial pressures exerted by each gas in the mixture. The total pressure of all gases in the anesthesia system at sea level is equivalent to approximately 760 mmHg (per unit of area). Although anesthetic gas monitors may display data expressed in millimeters of mercury (mmHg) or as volumes percent (vols%), it is important to understand how the measurement was made in principle. The reader should understand the difference between partial pressure (mmHg), which is an absolute term, and volumes percent, which is an expression of a proportion, or ratio.

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If the partial pressure of one component of a gas mixture is known, a reading in volumes percent can be computed as follows: Volumes % =

Partial pressure of the component gas (mmHg) Total pressure of all gases (mmHg)

× 100

Number of molecules (partial pressure) An analysis method that is based on quantifying a specific property of a gas molecule in effect determines in absolute terms the number of molecules of that gas that are present – that is, mmHg. Gas molecules that are composed of two or more dissimilar atoms (e.g. CO2 , N2 O, potent inhaled anesthetics) have bonds between their component atoms. Certain wavelengths of infrared radiation excite these molecules, stretching or distorting the bonds, which also absorb the radiation. Carbon dioxide molecules absorb infrared radiation at a wavelength of 4.3 ␮m. The greater the number of molecules of carbon dioxide present, the more radiation at 4.3 ␮m that is absorbed. This property of the carbon dioxide molecule is applied in the infrared carbon dioxide analyzer. Because the amount of infrared radiation absorbed is a function of the number of molecules present, it is, therefore, also a function of partial pressure. Thus, infrared analyzers measure partial pressure. In the analysis of gases by Raman spectroscopy (as was used in the now obsolete Ohmeda RASCAL II analyzer), a helium– neon laser emits monochromatic light at a wavelength of 633 nm. When this light interacts with the intramolecular bonds of specific gas molecules, it is scattered and re-emitted at wavelengths different from that of the incident monochromatic light. Each re-emission wavelength is characteristic of a specific gas molecule present in the gas mixture and therefore is a function of its partial pressure. Thus, Raman spectroscopy also measures partial pressures. A sufficient number of molecules of the gas(es) to be analyzed (i.e. adequate partial pressures) must be present to facilitate gas analysis by the infrared and Raman technologies. These systems must also be pressure-compensated if analyses are being made at ambient pressures other than those used for the original calibration of the systems.2

Measurement of proportion (volumes percent) Another approach to gas analysis is to separate the molecular component species of a gas mixture and determine what proportion (percentage) each gas contributes to the total (100%). This approach is applied in mass spectrometry. Thus, if in a sample of gas containing 100 molecules there were 21 molecules of oxygen, oxygen would represent 21 percent of the gas sample and therefore might reasonably be assumed to represent 21 percent of the original gas mixture. The result is expressed as 21 volumes percent, or as a fractional concentration (0.21). This technology does not measure partial pressures; it measures only proportions. If the system is provided with an absolute pressure

Chapter 14 – Respiratory Gas Monitoring

reading that is equivalent to 100 percent, the basic measured proportions can be converted to readings in mmHg. In the preceding example, if 100 percent were made equivalent to 760 mmHg, oxygen would have a calculated partial pressure of (760 × 21%) = 159 mmHg. These fundamental differences in the approaches to gas analysis and their basic units of measurement are important, particularly when the data displayed by these monitors are interpreted in a clinical setting and may affect patient management.

Gas analysis technologies Contemporary respiratory multigas analyzers use infrared spectroscopy to measure CO2 , N2 O, halothane, enflurane, isoflurane, desflurane, and sevoflurane. Oxygen is measured by a paramagnetic (rapid responding) analyzer or by a slow or fast responding fuel cell. Although certain technologies are no longer in common clinical use, it is worthwhile to briefly review some of them to appreciate their principles of operation.

Mass spectrometry For many anesthesia caregivers, the term “mass spec” is used as if it were synonymous with gas analysis. Indeed, many anesthetic record forms still (incorrectly) include the term MASS SPEC, but this technology has not been in routine clinical use for some years. It was, however, the first multigas monitoring system in widespread clinical use, following a description by Ozanne and colleagues in 1981.3 The mass spectrometer is an instrument that allows the identification and quantification, on a breath-by-breath basis, of up to eight of the gases commonly encountered during the administration of an inhalational anesthetic. These gases include oxygen, nitrogen, nitrous oxide, halothane, enflurane, and isoflurane; other agents, such as helium, sevoflurane, argon, and desflurane, could sometimes be added or substituted if desired. Although the technology of mass spectrometry had been available for many years, analyzer units dedicated to a single patient were too expensive for routine use in each operating room. In 1981, the concept of a shared, or multiplexed, system was introduced.3 This arrangement allowed one centrally located analyzer to function as part of a computerized multiplexed system that could serve up to 31 patient sampling locations (ORs and recovery room or intensive care unit beds) on a time-shared basis. The two multiplexed systems that became widely used were the Perkin-Elmer (later the Marquette Advantage System), and SARA (System for Anesthetic and Respiratory Analysis).

Principles of operation The mass spectrometer analyzer unit separates the components of a stream of charged particles (ions) into a spectrum according to their mass/charge ratios. The relative abundance of ions at certain specific mass/charge ratios is determined and is related

to the fractional composition of the original gas mixture. The creation and manipulation of ions is carried out in a high vacuum (10−5 mmHg) to avoid interference by outside air and to minimize random collisions among the ions and residual gases. The most common design of mass spectrometer was the magnetic sector analyzer, so called because it uses a permanent magnet to separate the ion beam into its component ion spectra (Figure 14.5). A stream of the gas to be analyzed is continuously drawn by a sampling pump from an airway connector via a long nylon catheter. During transit through the sampling catheter, the pressure decreases from atmospheric (usually 760 mmHg) in the patient circuit to approximately 40 mmHg by the inlet of the analyzer unit. A very small amount of the gas actually sampled from the circuit (approximately 10−6 mL/sec) enters the analyzer unit’s high-vacuum chamber through the molecular inlet leak. The gas molecules are then bombarded by an electron beam, which causes some of the molecules to lose one or more electrons and become positively charged ions. Thus an oxygen molecule (O2 ) might lose one electron and become an oxygen ion (O2 + ) with one positive charge. The mass/charge ratio (often termed m/z) would therefore be 32/1, or 32. If the oxygen molecule lost two electrons, it would gain two positive charges and the resulting ion (O2 2+ ) would have an m/z of 32/2, or 16. The process of electron bombardment also causes large molecules (e.g. halothane, enflurane, isoflurane) to become fragmented, or cracked, into smaller, positively charged ions. The positive ions created in the analyzer are then focused into a beam by the electrostatic fields in the ion source, directed through a slit to define an exact shape for the beam, and accelerated and directed into the field of the permanent magnet. The magnetic field influences the direction of the ions, causing each ion species to curve in a trajectory whose arc is related to its m/z. The effect is to create several separate ion beams exiting the magnetic field. The separated beams are directed to individual collectors, which detect the ion current and transmit it to amplifiers that create output voltages in relation to the abundance of the ion species detected by each collector. The collector plates are positioned so that an ion with a specific m/z ratio strikes a specific collector. The heaviest ions are deflected the least and travel the farthest before striking a collector (Figure 14.5). Collectors for these heavy ions are therefore located furthest from the ion source. Summing and other computer software measures the total voltage from all of the collector circuits as well as the individual voltages from each collector. Total voltage is considered equivalent to 100 percent of the analyzed gas mixture. Individual gas collector circuit voltages are expressed as percentages of the total voltage and displayed as percentages of the sampled gas mixture. Thus, if the voltage from the oxygen collector circuit (m/z 32) represented 30 percent of the total voltage from all of the collector circuits, oxygen would be read as constituting 30 percent of the total gas mixture analyzed. The Marquette Advantage and SARA systems used magnetic sector analyzers

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Figure 14.5. Schematic of a magnetic sector respiratory mass spectrometer. The respiratory gas is sampled and drawn over a molecular leak. Gas molecules enter a vacuum chamber (through the molecular inlet leak), in which they are ionized and electrically accelerated. A magnetic field deflects the ions. The mass and charge of the ions determine their trajectory, and metal dish collectors are placed to detect them. The electrical currents produced by the ions impacting the collectors are processed, the composition is computed, and the results are displayed.

GAS SAMPLE FROM PATIENT Molecular inlet leak “Light” ions PROXIMAL

Amplifier

N2-28

MAGNETIC FIELD

O2-32

CPU CO2-44

HIGH VACUUM

ISO frag . ENFL frag.

“Heavy” ions

HALO frag.

DISTAL

Collector plate

ION PUMP

that had up to eight collectors and therefore were able to detect and analyze up to eight different ion species, and thereby, parent gases. The mass spectrometer functions as a proportioning system for the components of a gas mixture. When it displays each of the components of the mixture as a percentage of the total, it makes the assumption that all the gases present have been detected. If ambient (atmospheric) pressure information is entered into the software, the measured percentages or proportions can be converted to readings in mmHg (i.e. partial pressures). Remember that the mass spectrometer does not measure partial pressures; it calculates them from the measured proportions and the atmospheric pressure information that must be supplied to it. Thus: Partial pressure (mmHg) = fractional concentration × total pressure. Usually, because the mass spectrometer was sampling respired gases from the patient circuit, the total pressure entered into the computer was ambient minus 47 mmHg, the latter representing the saturated vapor pressure of water at body temperature (37◦ C). Thus, at sea level (760 mmHg), a pressure of 713 mmHg would be entered into the mass spectrometer software to be apportioned among the gases present. The mass spectrometer readings, when displayed in mmHg, represent somewhat of a compromise because inspired gas is usually not fully saturated with water vapor, whereas expired gas usually is. If an incorrect value for total ambient pressure is entered into the mass spectrometer software, all readings in mmHg will be incorrect, but the readings in volumes percent will be correct. By way of an example, assume that the end-tidal carbon dioxide is measured as 5 percent by the mass spectrometer and that

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VACUUM PUMP

ambient pressure is 760 mmHg. The reading in mmHg will be 35.65 [i.e. (760 − 47) × 5%]. If a value of 500 mmHg is entered instead of 713 mmHg, the reading in mmHg will be 25 (i.e. 500 × 5%). In any case of doubt, the astute clinician would revert to the reading in volumes percent.

Shared (multiplexed) mass spectrometry systems Multiplexing permitted the sharing of one (expensive) mass spectrometer among up to 31 sampling locations or stations. In a shared system, the gas from each sampling location is directed in sequence by the multiplexing valve system to the mass spectrometer for analysis. The time between analyses at any particular location therefore depends on (1) the number of breaths analyzed from each sampling location (i.e. dwell time); (2) the number of sampling locations in use; (3) the priority settings; and (4) in the case of stat samples, the distance between sampling locations and the analyzer (up to 300 feet in some installations). Use of multiplexed mass spectrometry systems led anesthesia caregivers to appreciate the value of respiratory gas monitoring, as well as the limitations, the main one being that they were shared and that the data were updated only intermittently. In October 1986, the American Society of Anesthesiologists (ASA) first approved standards for basic intraoperative monitoring. As the standards evolved, the requirement for continuous capnometry was not met by a shared mass spectrometry system. The systems were expensive to install and maintain, and were not always easily upgradable when the new agents desflurane and sevoflurane were introduced. In addition, the long sampling catheters, combined with rapid respiratory rates, led to significant artifacts; the sampling pump could cause significant negative pressure in the breathing system, and when the system failed, all of the monitored sites were affected.4,5

Chapter 14 – Respiratory Gas Monitoring

Practitioners demanded continuous gas monitoring. The most important functions of a multiplexed mass spectrometry system could be served by other dedicated gas monitors, and the multiplexed mass spectrometer-based systems became extinct.

Dedicated (stand-alone) mass spectrometry systems A number of smaller stand-alone mass spectrometers were developed (e.g. Ohmeda 6000; Ohmeda, Madison, WI) for dedicated single-patient use. The Ohmeda 6000 Multigas Analyzer was a quadrupole filter type of mass spectrometer. It worked on the principle that a controlled electrostatic field can prevent all but a narrow range with regard to mass/charge ratio of charged particles (ions) from reaching a target. In the Ohmeda 6000 unit, the gas sampling rate was fixed at 30 mL/ min. One potential advantage of a quadrupole system is that it could be adapted to measure new or additional agents by changes in software only. A number of other stand-alone quadrupole filter mass spectrometers were marketed but, owing to cost and reliability issues, their production was discontinued.

Infrared analysis The infrared (IR) spectrum ranges between wavelengths 0.40 and 40 ␮m. Measurement of the energy absorbed from a narrow band of wavelengths of IR radiation as it passes through a gas sample can be used to measure the concentrations of certain gases. Asymmetric, polyatomic, polar molecules, such as carbon dioxide, nitrous oxide, water, and the potent volatile anesthetic agents absorb IR energy when their atoms rotate or vibrate asymmetrically, resulting in a change in dipole moment (i.e. the charge distribution within the molecule). The nonpolar molecules argon, nitrogen, helium, xenon, and oxygen do not absorb IR energy. Because the number of gas molecules in the path of the IR energy beam determines the total absorption, IR analyzers measure the partial pressure. Carbon dioxide, nitrous oxide, and anesthetic gases exhibit absorption of radiation at unique bands in the IR spectrum (Figure 14.6). Carbon dioxide molecules absorb strongly between 4.2 and 4.4 ␮m, whereas nitrous oxide molecules absorb strongly between 4.4 and 4.6 ␮m and less strongly at 3.9 ␮m. The potent volatile anesthestic agents have strong absorption bands at 3.3 ␮m and throughout the range of 8 to 12 ␮m. The close proximity of the nitrous oxide and carbon dioxide absorption bands may cause some carbon dioxide analyzers to be affected by high concentrations of nitrous oxide.6,7 This phenomenon is called collision or pressure broadening because molecular collisions result in a change in the dipole moment of the gas being analyzed. Thus the IR absorption band is broadened and the apparent absorption at the measurement wavelength may be altered. In a typical IR carbon dioxide analyzer, 95 percent oxygen causes a 0.5 percent decline in the measured carbon dioxide. Nitrous oxide causes a more substantial increase of about 0.1 percent carbon dioxide per 10 percent

Figure 14.6. Absorption bands of respiratory gases in the infrared spectrum. (From Raemer DB. Monitoring respiratory function. In Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and Practice of Anesthesiology, St. Louis: Mosby-Year Book,1992, with permission.)

nitrous oxide because of collision broadening. Contemporary multigas analyzers automatically compensate for the effect of collision broadening by measuring the concentrations of interfering gases. A simple IR analyzer (Figure 14.7) consists of a heated black body radiator that is the source of IR radiation, a sample cell (or cuvette) through which the gas to be analyzed is drawn by a sampling pump, and a detector that generates an output signal related to the intensity of the IR radiation that is detected. (A black body radiator is a theoretical object that is totally absorbent to all thermal energy that falls on it; thus, it does not reflect any light and so appears black. As it absorbs energy, it heats up and reradiates the energy as electromagnetic IR Source

Gas Sample in

Gas Sample out

Gas cuvette

IR Detector

Filter Single-beam single filter infrared analyzer Figure 14.7. Diagram of a simple single-wavelength IR respiratory gas analyzer. An IR source emits a beam that passes through a filter, which passes only the wavelength absorbed by the gas of interest. The respiratory gas from the patient is sampled and passes through the gas cell in the optical path. An IR detector measures intensity of the IR wavelength that has passed through the gas sample. The intensity is inversely related to the partial pressure of that gas in the sample cell. The electrical signal from the detector is processed to report the gas composition in mmHg (or in kilopascals, abbreviated kPa; 1 kPa is equivalent to 7.5 mmHg). This value can be converted (automatically) to a reading in volumes percent if the ambient pressure is known.

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radiation.) A narrow bandpass filter, which allows only radiation at the wavelength of interest to pass through, is interposed between the IR source and the cuvette, or between the cuvette and the detector. The intensity of radiation reaching the detector is inversely related to the concentration of the specific gas being measured. A number of sources of IR radiation can be used to produce a broad spectrum of IR radiation. Light sources made of tungsten wires or ceramic resistive materials heated to 1500 to 4000 K emit energy over a broad wavelength range that includes the absorption spectra of the respiratory gases. The radiation may be pulsed electronically, or if constant, may be made intermittent by being interrupted (“chopped”) mechanically. Because energy output of IR light sources tends to drift, optical systems have been designed to stabilize the analyzers. Three common designs are distinguished by their use of single or dual IR beams and by their use of positive or negative filtering.8

Single-beam positive filter In one single-beam positive filter design, precision optical bandpass filters mounted on a chopper wheel spinning at 40 to 250 revolutions per minute sequentially interrupt a single IR beam. The beam retains energy at a narrow band of wavelengths during each interruption. For each gas of interest, a pair of bandpass filters are selected at an absorption peak and at a reference wavelength where relatively little absorption occurs. The chopped IR beam then passes through a cuvette containing the sample gas. The ratio of intensity of the IR beam for each pair of filters is proportional to the partial pressure of the gas and is insensitive to changes in the intensity of the IR source.

Single-beam negative filter In the single-beam negative filter design, the filters are usually gas-filled cells mounted in a spinning wheel. During each interruption, the IR beam retains energy at all wavelengths except those absorbed by the gas. The chopped IR beam then passes through a cuvette containing the sample gas. Analogous to the positive filter design described previously, the ratio of IR beam intensity for each pair of filter cells is proportional to the partial pressure of the gas and is insensitive to changes in intensity of the IR source.

Dual-beam positive filter In the dual-beam positive filter design, the IR energy from the source is split into two parallel beams. One beam passes through the sample gas, and the other passes through a reference gas. A spinning blade passes through the beams and sequentially interrupts one, the other, then both. The two beams are optically focused to a single point, at which a bandpass optical filter selected at the absorption peak of the gas of interest is mounted over a single detector. As before, the ratios of the intensities of

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the sample and reference beams are proportional to the partial pressure of the gas.

Detectors of infrared radiation To measure carbon dioxide, nitrous oxide, and sometimes anesthetic agents, a radiation-sensitive solid state material, lead selenide, is commonly used as a detector. Lead selenide is quite sensitive to changes in temperature; therefore, it is usually thermostatically cooled or temperature-compensated. Anesthetic agents, carbon dioxide, and nitrous oxide are sometimes measured with another detector type, the Luft cell. This detector uses a chamber filled with gas that expands as IR radiation enters the chamber and is absorbed. A flexible wall of the chamber acts as a diaphragm that moves as the gas expands, and a microphone converts the motion to an electrical signal. The signal processor converts the measured electrical currents to display gas partial pressure. First, the ratios of detector currents at various points in the spinning wheel’s progress (or from multiple detectors) are computed. Next, electronic scaling and filtering are applied. Finally, linearization, according to a look-up table containing the point-by-point conversion from electrical voltage to gas partial pressure, is accomplished by a microprocessor. Compensation for cross-sensitivity or interference between gases can be accomplished by the microprocessor following linearization.

Infrared wavelength and anesthetic agent specificity Infrared analyzers must use a specific wavelength of radiation according to the absorbance peak of each gas to be measured. Thus, carbon dioxide is measured using a wavelength of 4.3 ␮m and nitrous oxide using 3.9 ␮m. Older agent analyzers (e.g. the Datex Capnomac)9 used a wavelength of 3.3 ␮m to measure the potent inhaled anesthetics, but use of a single wavelength did not permit differentiation among the agents. When such a system is used, the analyzer must be programmed by the user for the particular agent being administered. This action sets the appropriate gain in the software program, and the displayed reading will be accurate for the one agent in use. Obviously, programming such an analyzer for the wrong agent, or use of mixed agents, leads to erroneous readings of anesthetic agent concentration. Modern IR analyzers are agent-specific (i.e. they have the facility to both identify and quantify mixed agents in the presence of one another) by measuring each agent at a separate specific wavelength. Contemporary analyzers that can identify and quantify anesthetic agents incorporate individual wavelength filters in the range of 8 to 12 ␮m. An example is the Datex-Ohmeda Compact Airway Module (GE Healthcare) (Figures 14.1, 14.2, and 14.8), which is a nondispersive (i.e. with no provision for dispersing the emitted radiation into its

Chapter 14 – Respiratory Gas Monitoring

Nondispersive IR analyzer

IR absorbance of AAs

IR Source

Sample chamber

Thermopile detectors

Absorbance (arbitrary units)

Temp sensor

Desflurane

Enflurane Halothane

Desflurane

Sample gas out

Sample gas in

7 wavelengths

3.3

Figure 14.8. Principles of GE/Datex-Ohmeda IR analyzer in the Compact Airway Module. In this design, the IR beam is interrupted electronically rather than mechanically by a “chopper” wheel. From ref. 10, by permission of GE Datex-Ohmeda.

5.0 Wavelength (μm)

10.0

Figure 14.10. Principles of GE/Datex-Ohmeda IR analyzer in Compact Airway Module. Absorbance bands for the potent inhaled anesthetic agents. From ref. 10, by permission of GE Datex-Ohmeda.

component wavelengths) IR analyzer that measures the absorption of the gas sample at seven different wavelengths, which are selected using optical narrow band filters. The IR radiation detectors are thermopiles. Carbon dioxide and N2 O are calculated from absorption measured at 3 to 5 ␮m (Figure 14.9). Identification and calculation of the concentrations of anesthetic agents are made by measuring absorption at five wavelengths in the 8 to 9 ␮m band and solving for the concentrations from a set of five equations (Figure 14.10).10 A schematic of a multiwavelength analyzer in which the beam of radiation is interrupted mechanically (chopped) is shown in Figure 14.11.

polymer that selectively allows water vapor to pass from its interior to the relatively dry exterior, is commonly used to eliminate water vapor. In addition, a water trap is usually interposed between the patient sampling catheter and the analyzer to protect the optical system from liquid water and body fluids (Figure 14.1). One design of sampling tubing (Nomoline, see Figure 14.4) incorporates a water separation section and bacterial filter that removes both water and liquid water from the sampled gas flow.

Sampling systems and infrared analysis

The photoacoustic spectrometer (Figure 14.12) is similar to the basic IR spectrometer. Infrared energy is passed through optical filters that select narrow-wavelength bands corresponding to the absorption characteristics of the respired gases. Carbon dioxide is measured at a wavelength of 4.3 ␮m, nitrous oxide at 3.9 ␮m, and the potent inhaled agents at a wavelength between 10.3 and 13.0 ␮m.11 Evenly spaced windows are located along the circumference of a rotating wheel. The optical components are located astride the wheel along one of its radii. A series of IR beams pulse on and off at particular frequencies, according to the rate of rotation of the wheel and the spacing of the windows. The gas flowing through the measurement cuvette is exposed to the pulsed IR beams. As each gas absorbs the pulsating IR energy in its absorption band, it expands and contracts at that frequency. The resulting sound waves are detected with a microphone. The partial pressure of each gas in the sample is then proportional to the amplitude (or volume) of the measured sound. The photoacoustic technique has the distinct advantage over other IR methods in that a simple microphone detector can be used to measure all the IR-absorbing gases. However, this device is sensitive to interference from loud noises and vibration. Also, because only one wavelength is used to measure the potent inhaled anesthetics, this monitor is unable to distinguish among the agents and requires that it be programmed for the one that is in use. Erroneous readings might arise in the presence of mixed anesthetic agents. This technology was used in the

Sidestream sampling analyzers continuously withdraw between 50 and 250 mL/min from the breathing circuit through narrow-gauge sample tubing to the optical system, where the measurement is made. One of the disadvantages of sidestream monitors is the need to deal with liquid water and water vapor. Water vapor from the breathing circuit condenses on its way to the sample cuvette and can interfere with optical transmission. Nafion tubing (PermaPure, Toms River, NJ), a semipermeable

Absorbance (arbitrary units)

Absorbances of CO2 and N2O

N2O

CO2 Filter Filter

0 4.0

4.5 Wavelength (μm)

Figure 14.9. Principles of GE/Datex-Ohmeda IR analyzer in Compact Airway Module. Absorbance bands used for CO2 and N2 O. From ref. 10, by permission of GE Datex-Ohmeda.

Infrared photoacoustic spectrometer

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O2-measuring cell

Water trap

Buffer Patient

Pump

Flow sensor

Valves Electronic evaluation

Sample gas return

Monitoring in Anesthesia and Perioperative Care

Flow controller Ambient air Valves

Photoelectric barrier

Pressure

Temperature

Heater Analog amplifier A/D–converter

Electronic control

Processor system

Patient monitor

Figure 14.11. Schematic of multiwavelength IR analyzer with mechanical interruption (“chopping”) of IR beam. Courtesy of Dr¨ager Medical, Telford, PA.

Chopper wheel

Microphone

Multigas signal

Motor Switched magnetic field

Gas outlet

Measurement chamber Pump Optical filter IR light source

Flow regulation

Patient gas inlet

Microphone

O2 reference signal

O2 reference gas inlet

Figure 14.12. Schematic diagram of a photoacoustic spectrometer. An IR source emits a beam which passes through a spinning chopper wheel that has several rows of circumferential slots. The interrupted IR beams then pass through optical filters that select specific wavelengths of light chosen to be at the absorption peaks of the gases to be measured. Each interrupted IR light beam impinges on its respective gas in the measurement chamber, causing vibration of the gas as energy is absorbed and released from the molecules. The vibration frequency of each gas depends on the spacing of its slots on the chopper wheel. A microphone converts the gas vibration frequencies and amplitudes into electrical signals that are converted to the gas concentrations for display. (From Raemer DB. Monitoring respiratory function. In Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and Practice of Anesthesiology, St. Louis: Mosby-Year Book, 1992, with permission.)

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A

B Figure 14.13. (A) Mainstream multigas analyzer module that measures CO2 , N2 O, and anesthetic agents. (B) Same as (A) but with additional ultrafast oxygen sensor. IRMA Phasein AB, Danderyd, Sweden.

Bruel and Kjaer Anesthetic Gas Monitor 1304. It is the technology that is currently used in the Innova 1412 Field Gas Monitor used for monitoring traces gases (Luma Sense Technologies, California Analytical Instruments, Orange, CA).

room temperature, about one-millionth of the energy is scattered at a longer wavelength, producing a so-called red-shifted spectrum. This Raman scattering can be used to measure the constituents of a gas mixture. Unlike IR spectroscopy, Raman scattering is not limited to gas species that are polar. Carbon dioxide, oxygen, nitrogen, water vapor, nitrous oxide, and the potent volatile anesthetic agents all exhibit Raman activity. Monatomic gases such as helium, xenon, and argon, which lack intramolecular bonds, do not exhibit Raman activity. The medical Raman spectrometer uses a helium–neon laser (wavelength 633 nm, or 0.633 ␮m) to produce the incoming monochromatic light beam. The Raman scattered light is of low intensity and measured perpendicular to the laser beam. The measurement cuvette is located in the cavity of the laser so the gas molecules are struck repeatedly by the beam (Figure 14.15). This results in enough Raman scattering to be collected and processed by the optical detection system. Photomultiplier tubes count the scattered photons at the characteristic Raman-shifted wavelength for each gas. Thus the Raman spectrometer measures the partial pressures of the gases in its measurement cuvette. Measurements are converted electronically to the desired units of measure and displayed on the screen. Raman spectroscopy is the principle of operation of the Ohmeda RASCAL II monitor (Ohmeda; Boulder, CO). The RASCAL II Raman spectrometer had the same capabilities as the mass spectrometer. In particular, it was able to measure nitrogen for detection of air embolism. Unfortunately, despite its obvious versatility, this monitor is no longer in production, although many are still in use.

Mainstream multigas analysis Mainstream multigas IR analysis has recently been introduced by Phasein (Danderyd, Sweden) in its IRMA series of multigas analyzers. The entire IRMA mainstream probe weighs only 30 g and measures IR light absorption at ten different wavelengths to precisely determine gas concentrations in the mixture (Figure 14.13A). A selection of disposable airway adapters is available for different clinical applications. The probe comprises all the necessary components required for advanced signal processing, along with a comprehensive digital RS232 interface. The probes are universally calibrated and deliver processed data for display on the screen of any display monitor. The same miniaturized technology is used in Phasein’s EMMA Emergency Capnometer, a device that displays respiratory rate and incorporates apnea, high CO2 , and low CO2 audible and visual alarms (Figure 14.14).

Raman spectroscopy When light strikes gas molecules, most of the energy scattered is absorbed and re-emitted in the same direction and at the same wavelength as the incoming beam (Rayleigh scattering).12 At

Figure 14.14. EMMA Capnocheck Mainstream capnometer Plug-in and Measure Multigas Technologies, Phasein AB, Danderyd, Sweden.

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Monitoring in Anesthesia and Perioperative Care

Gas sample He Ne laser

Gas cell

Gas filters

Counting circuits

Computer Digital counts

Figure 14.15. Diagram of a Raman scattering respiratory gas analyzer. A laser tube generates a monochromatic (633 nm) light beam that is contained within a cavity by mirrors. The respiratory gas from the patient is sampled and passes through the laser beam. The gas molecules scatter a small amount of light at wavelengths different from that of the incoming beam. The wavelength shift is characteristic of the gas species. The scattered light is detected, and the gas composition is computed and displayed to the user in the appropriate units of measure.

Microstream capnography technology Microstream is a relatively new approach to capnometry that uses a novel laser-based technology called molecular correlation spectroscopy (MCS) as the infrared emission source.13 This produces a highly efficient and selective emission of a spectrum of discrete wavelengths that exactly match those for CO2 absorption. One of the major problems of conventional nondispersive IR technology is that the black body emitter produces a very broad IR spectrum, most of which is redundant to CO2 monitoring, and must be removed using optical interference filters. Such filters are limited in their ability to remove radiation that falls between the discrete absorbing lines. Microstream technology uses an MCS source that operates at room temperature (unlike the black-body emitters) and emits only CO2 -specific radiation of approximately 100 discrete lines in the region of 4.2 to 4.35 ␮m. This permits use of a smaller sample cell (15 ␮L) and a gas sampling flow rate of 50 mL/min. The technology was initially developed by Oridion (Oridion Microstream; Needham, MA) but is now used (through licensing partnerships) in many other brands of capnograph (e.g. Spacelabs, Dr¨ager, Philips). The small size, low power requirement, small sample cell size, low gas sampling flow rate, rapid response time, short warmup time, CO2 specificity, and no need for routine calibration make this technology particularly useful in portable carbon dioxide monitors.14

Water vapor and accuracy of capnometers Water vapor may be an important factor in the accuracy of a carbon dioxide analyzer. Most sidestream carbon dioxide analyzers report ambient temperature and pressure, dry (ATPD) values for PCO2 by using a water trap and Nafion (water

160

vapor permeable) tubing to remove water vapor from the sample. It has been recommended that carbon dioxide analyzers report their results at body temperature and pressure, saturated (BTPS), so end-tidal values are close to conventionally reported alveolar gas partial pressure.15 The error in reporting PCO2 at ATPD when it should be reported at BTPS is about 2.5 mmHg. Carbon dioxide values reported in ATPD can be converted to BTPS by decreasing the dry gas reading by the fraction (PATM − 47)/PATM , where PATM is the atmospheric pressure in mmHg and 47 mmHg is the vapor pressure of water at 37◦ C. Mainstream sampling analyzers naturally report readings near BTPS. Depending on breathing circuit conditions, a small decrease from body temperature may result in the analyzer reading slightly less than BTPS values. Condensation of water can affect the windows of the mainstream airway adapter and cause erroneous readings. These adapters are therefore heated or otherwise designed to prevent condensation.

Colorimetric carbon dioxide detectors Carbon dioxide in solution is acidic; therefore, pH-sensitive dyes can be used to detect and measure its presence. A colorimetric carbon dioxide detector is designed to be interposed between the tracheal tube and the breathing circuit. Respired gas passes through a hydrophobic filter and a piece of filter paper that is visible through a plastic window. The originally described detector (FENEM FEF CO2 Detector) consisted of a piece of filter paper permeated with an aqueous solution containing metacresol purple, a pH-sensitive dye. Carbon dioxide from the exhaled breath dissolves in the aqueous solution, changing the color of the dye from purple to yellow. The degree of color change is dependent on the concentration of carbon dioxide. On inspiration of carbon dioxide-free gas, carbon dioxide leaves the solution and the color of the indicator returns to its resting (purple) state.16 A number of colorimetric devices are now commercially available for use in adult and pediatric patients. They may use other CO2 -sensitive dyes and are calibrated to provide an approximate indication of expired carbon dioxide concentration that can be discerned by comparison of the indicator color with a graduated color scale printed on the device’s housing. For example, the Easy Cap II (Covidien-Nellcor, Boulder, CO) color changes from purple to yellow, indicating 2 percent to 5 percent (15–38 mmHg) carbon dioxide with each exhaled breath. On inspiration, the color should change back to purple, indicating absence of CO2 in the inspired gas (Figure 14.16). A permanent change in color may mislead the uneducated user;17,18 hence the following caution in the directions for use from the manufacturer of the Easy Cap II CO2 detector: “Interpreting results before confirming six breath cycles can yield false results. Gastric distension with air prior to attempted intubation may introduce CO2 levels as high as 4.5% into the Easy Cap detector if the endotracheal tube is misplaced in the esophagus. Initial Easy Cap detector color (yellow) may be interpreted as a false positive if read before delivery of six breaths.” The warnings also

Chapter 14 – Respiratory Gas Monitoring

Figure 14.16. Nellcor Easy Cap II CO2 detector. Left: Purple = No. little CO2 ; Right: Yellow = 5% CO2 . Tyco Healthcare, Boulder, CO.

further include a statement, “Reflux of gastric contents, mucus, edema fluid, or intratracheal epinephrine into the Easy Cap can yield persistent patchy yellow or white discoloration which does not vary with the respiratory cycle. Contamination of this type may also increase airway resistance and affect ventilation. Discard device if this occurs.” This type of detector is intended to be used to confirm clinical signs of tracheal intubation when conventional capnography is not available. Both adult and pediatric versions are commercially available. The newest FENEM CO2 indicator is designed to be attached to the exhalation port (30 mm or 19 mm) of a self-inflating resuscitator bag, where it does not add dead space or resistance to flow. Another version of the colorimetric CO2 detector, the CO2NFIRM NOW CO2 Detector (Kendall, Tyco Healthcare; Mansfield, MA), is marketed as a device to confirm intragastric placement of an orogastic or nasogastric tube to prevent intratracheal placement.

Oxygen analyzers In all contemporary anesthesia delivery systems, the fraction of inspired oxygen (FIO2 ) in an anesthesia breathing circuit is monitored by an oxygen analyzer. Two types of oxygen analyzers are in common use for monitoring: those based on a fuel or galvanic cell principle, and paramagnetic (Pauling) sensors. In the past, in addition to these methods, multigas analyzers using mass spectroscopy or Raman spectroscopy to measure oxygen were also used as oxygen monitors (see previous discussion).

Fuel cell The fuel cell or galvanic cell is basically an oxygen battery consisting of a diffusion barrier, a noble metal (gold mesh or platinum) cathode, and a lead or zinc anode in a basic (usually potassium hydroxide) electrolyte bath (Figures 14.17 and 14.18). The sensor, covered by an oxygen-permeable membrane, is exposed to the breathing circuit. Oxygen diffusing into the Figure 14.17. Fuel cell oxygen analyzer. GE DatexOhmeda, Madison, WI.

Fuel cell

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Electronics and display

used to monitor the average oxygen concentration in the inspiratory limb of the breathing system. An ultrafast galvanic oxygen sensor will be available for the mainstream multigas analyzer (Figure 14.13B). This is specified to have a response time of ⬍300 msec, enabling breath-by-breath oxygen analysis.

Voltmeter

Temperature compensation

Paramagnetic oxygen analyzer

KOH Electrolyte Thermistor Lead anode

O2+2 Pb+2 OH–=2 PbO2H–

Noble metal cathode

O2 O2 O2 O2 O2 O2 O2 O2 O2

O-ring seal O2-permeable membrane O2 O2 O2 O2 O2 O2 O2

O2

O2

Figure 14.18. Principles of fuel cell oxygen analyzer. Oxygen in the gas sample permeates a membrane and enters a potassium hydroxide electrolyte solution. An electrical potential is established between a lead anode and noble metal cathode as oxygen is supplied to the anode. The measured voltage between the electrodes is proportional to the oxygen tension of the gas sample. Temperature compensation is required for accurate measurement. (From Raemer DB. Monitoring respiratory function. In Rogers MC, Tinker JH, Covino BG, Longnecker DE, eds. Principles and Practice of Anesthesiology, St. Louis: Mosby-Year Book, 1992, with permission.)

sensor is reduced to hydroxyl ions at the cathode, according to the following reaction: O2 + 2 H2 O + 4 e− → 4 OH−

The oxygen molecule has two electrons in unpaired orbits, which makes it paramagnetic (i.e. susceptible to attraction by a magnetic field). Most other gases are weakly diamagnetic and repelled. The paramagnetic oxygen sensor uses the strong, positive magnetic susceptibility of oxygen in a pneumatic bridge configuration to determine oxygen concentration by measuring a pressure differential between a stream of reference gas (room air at about 10 mL/min) and one of the measured gas as the two streams are exposed to a changing magnetic field (Figure 14.19). An electromagnet is rapidly switched off and on (at a frequency of 165 Hz in the GE compact airway module10 ), creating a rapidly changing magnetic field between its poles. The electromagnet is designed to have its poles in close proximity, forming a narrow gap. The streams of sample and reference gas have different oxygen partial pressures, and the pressure between the entrance and exit of the respective gas streams differs slightly because of the magnetic force on the oxygen molecules. This generates sound waves from each gas stream. A sensitive pressure transducer (i.e. a microphone) is used to convert the sound waves to an electrical signal. The output signal is proportional to the oxygen partial pressure difference between the two gas streams and should be displayed as the PO2 but is more usually displayed as the equivalent concentration in volumes percent. Paramagnetic oxygen analysis is used in most contemporary multigas analyzers. The main advantage of paramagnetic analysis over the standard fuel cell is that it has a very rapid response, permitting continuous breath-by-breath monitoring of the respired oxygen

The hydroxyl ions then oxidize the lead (or zinc) anode, and the following reaction occurs at the anode: 2 Pb + 6 OH− → 2 PbO2 H− + 2 H2 O + 4 e− The flow of current depends on the uptake of oxygen at the cathode (according to Faraday’s first law of electrolysis), and the voltage developed is proportional to the oxygen partial pressure. No polarizing potential is needed because the cell produces its own. The fuel cell sensor voltage is measured and electronically scaled to units of partial pressure or equivalent concentration (in volumes percent) and displayed as a readout. Similar to any battery, the fuel cell has a limited lifespan, depending on its period of exposure to oxygen. For this reason, machine manufacturers have recommended that the cell be removed from the breathing system when not in use. The response time of conventional fuel cell O2 analyzers is slow; therefore, they are best

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Figure 14.19. Paramagnetic oxygen analyzer. The sample and reference gas streams converge in a rapidly changing magnetic field. Because the two streams have different oxygen tensions (i.e. different numbers of oxygen molecules), a pressure differential is created across a sensitive pressure transducer. The transducer converts this force to an electrical signal that is displayed as oxygen partial pressure or converted to a reading in volumes percent.

Chapter 14 – Respiratory Gas Monitoring

air. It must be remembered that the fuel cell is actually measuring the ambient PO2 (normally 159 mmHg in dry air at sea level) but for convenience displays 21 volumes percent. Therefore, if a fuel cell that has been calibrated to read 21 percent at sea level is then used at a much higher altitude, the readout will show less than 21 percent (because the ambient PO2 is lower), even though the composition of the atmosphere is still 21 percent oxygen by volume. The gain of the paramagnetic sensor changes with temperature, humidity, and pneumatic factors. The contemporary paramagnetic oxygen analyzers perform their own periodic computer-controlled automated calibration process.

CAPNOGRAM 38 mmHg

0 mmHg 21% O2

16% O2

OXYGRAM Figure 14.20. Capnogram (above) and oxygram (below). The latter is almost a mirror image of the capnogram.

concentration. The graphical representation of this can be displayed as the oxygram, which is essentially a mirror image of the capnogram (Figure 14.20). Normally, the gas exiting the multigas analyzer is directed to the waste gas scavenging system of the anesthesia delivery system. If a low-flow or closed-circuit anesthesia technique is being used, the gas exiting the analyzer is usually returned to the breathing system. In this case, it must be remembered that nitrogen from the room air reference gas stream is also being added, albeit at a low rate (8 mL/min), and will accumulate in the breathing circuit.

Calibration of oxygen analyzers Oxygen analyzers require periodic calibration. Because all analyzers produce an electrical signal that is proportional to oxygen partial pressure, the constant of proportionality (gain) must be determined. Generally, the electrical signal in the presence of 0 percent oxygen is known to be near zero; therefore, no offset correction is required. In the fuel cell, the gain changes over time because of changes in the electrolyte, electrodes (the anode is sacrificial), and membrane. The anesthesia caregiver must therefore calibrate it to read 21 percent by removing it from the breathing system and allowing equilibration in room

Table 14.1.

Gases in the anesthesia delivery system can be analyzed via a number of modern technologies, each of which is based on application of some specific physical property of the gas molecule. The analysis methods and their applications are summarized in Table 14.1. In interpreting gas analysis data, it is important to understand the principles of how the data were obtained so erroneous data can be identified and, if necessary, rejected.

Balance gas Contemporary multigas analyzers measure the partial pressure of each gas of interest in a dry gas mixture. The PO2 is measured by paramagnetic analysis, and PN2 O, PCO2 , and Panesthetic agent by IR technology. If the sum of these partial pressures is subtracted from the ambient barometric pressure, the result is the partial pressure(s) of unmeasured gas(es) and may be displayed as balance gas (Figure 14.21). In most cases, the balance gas is nitrogen; in the absence of a specific nitrogen gas analyzer (i.e. Raman or mass spectrometer), it has been described as the “poor man’s nitrogen.” However, if a heliox (75% helium/25% oxygen) mixture were being analyzed, helium would be read as the balance gas.

Nitric oxide Inhaled nitric oxide (NO) is used to treat hypoxemia and pulmonary hypertension associated with acute respiratory failure. A number of NO delivery systems are commercially available, and incorporate or require contemporaneous use of a nitric oxide analyzer.

Gas monitoring technologies Gas

Technology Mass spec Raman IR light IR acoustic Fuel cell Paramagnetic Moleculare correlation spectroscopy

O2

CO2

N2 O

AA specific

N2

He

Ar

x x

x x x x

x x x x

x x x x

x x

x

x

x x x

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Monitoring in Anesthesia and Perioperative Care

Applications of gas monitoring Oxygen

Figure 14.21. Screen of GE Datex-Ohmeda S5 monitor showing balance gas concentration and MAC value.

The INOvent delivery system (GE/Datex-Ohmeda) delivers NO in concentrations of 0 to 40 ppm. Circuit gas is sampled at a rate of 230 mL/min and analyzed electrochemically (amperometric approach) when NO reacts with an electrode to induce a current or voltage change. The measurement ranges are 0 to 100 ppm for NO, and 0 to 15 ppm for nitrogen dioxide, NO2 . The concentration of NO can also be determined using a simple chemiluminescent reaction involving ozone.19 Chemiluminescence is the emission of light with limited emission of heat (luminescence), as the result of a chemical reaction. A sample containing nitric oxide is mixed with a large quantity of ozone. The nitric oxide reacts with the ozone to produce oxygen and nitrogen dioxide. This reaction also produces light (chemiluminescence), which can be measured with a photodetector. The amount of light produced is proportional to the amount of nitric oxide in the gas sample. NO + O3 → NO2 + O2 + light To determine the amount of nitrogen dioxide (NO2 ) in a sample (containing no NO), it must first be converted to nitric oxide (NO) by passing the sample through a converter before the ozone activation reaction is applied. The ozone reaction produces a photon count proportional to NO, which is proportional to NO2 before it was converted to NO. In the case of a mixed sample containing both NO and NO2 , the preceding reaction yields the amount of NO and NO2 combined in the gas sample, assuming that the sample is passed through the converter. If the mixed sample is not passed through the converter, the ozone reaction produces activated NO2 only in proportion to the NO in the sample. The NO2 in the sample is not activated by the ozone reaction. Although unactivated NO2 is present with the activated NO2 , photons are emitted only by the activated species, which is proportional to the original NO. The final step is to subtract NO from (NO + NO2 ) to yield NO2 .19

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The qualitative and quantitative oxygen-specific analyzer in the anesthesia breathing system is probably the most important of all the monitors on the anesthesia workstation. Prior to the general use of an oxygen analyzer in the anesthesia breathing system, a number of adverse outcomes resulting from unrecognized delivery of a hypoxic gas were reported.20 To be used correctly, the oxygen analyzer must be calibrated and appropriate low and high audible and visual concentration alarm limits set. This analyzer, sampling gas in the inspiratory limb of the breathing system or at the Y-piece, is the only means of ensuring that oxygen is actually being delivered to the patient. In the event that a hypoxic gas or gas mixture is delivered, the alarm will sound. Such situations can occur if there is a pipeline crossover (e.g. O2 for N2 O), an incorrectly filled oxygen storage tank or cylinder, or failure of a proportioning system intended to prevent delivery of a gas mixture containing less than 25 percent oxygen. The high oxygen concentration alarm limit is important when caring for patients for whom a high oxygen concentration may be harmful, such as premature infants and patients treated with chemotherapeutic drugs (e.g. bleomycin), who are more susceptible to oxygen toxicity. Continuous monitoring of inspired and end-expired oxygen is very helpful in assuring completeness of preoxygenation of the lungs before a rapid-sequence induction of anesthesia or in patients at increased risk for hypoxemia during induction of anesthesia, such as the morbidly obese. During preoxygenation, nitrogen is washed out of the lungs and is replaced by oxygen.21 Preoxygenation is ideal when the inspired oxygen concentration is 100 percent and the end-tidal O2 is 95 percent, the difference of 5 percent being the exhaled CO2 . The rapid-response oxygen analyzer makes possible the display of the oxygram, a continuous real-time display of oxygen concentration on the y-axis, against time on the x-axis (Figure 14.20). Now that it is possible to accurately measure inspiratory and expiratory gas flows and, therefore, volumes (i.e. flow = volume/time), by the airway, the oxygram can be combined with these flow signals to plot inspired and expired oxygen concentrations against volume.10 In theory, the integral of simultaneous flow and oxygen concentration during inspiration and expiration is the inspired and expired volume of oxygen. From the difference between these two amounts, oxygen consumption can be estimated. Barnard and Sleigh used this method (with a Datex Ultima monitor) to measure oxygen consumption in patients under general anesthesia and compared it with that obtained simultaneously using a metabolic monitor.22 These authors concluded that the Datex Ultima may be used with moderate accuracy to measure oxygen uptake during anesthesia. The analogous plot for the capnogram allows measurement of carbon dioxide production. The application of this concept is termed indirect calorimetry and is used in the GE bedside metabolic module.23 By monitoring flow and measuring the gas concentrations, this module

Chapter 14 – Respiratory Gas Monitoring

Table 14.2.

Capnogram abnormalities

Abnormality

Possible causes

1. Absent

Capnograph line disconnect No ventilation, circuit obstructed Esophageal intubation, tube misplaced

2. End-tidal increased Inspired CO2 zero

Increased production (fever, MH, tourniquet or X-clamp release, bicarbonate, CO2 administration)

Inspired CO2 increased

3. End-tidal decreased

Figure 14.22. Screen of GE Datex-Ohmeda S5 Compact Airway Module monitor showing metabolic monitoring data (VO2 , VCO2 , RQ) from integrating concentration and flow signals.

provides measurements of O2 consumption (VO2 ) and CO2 production (VCO2 ), and calculates respiratory quotient and energy expenditure (Figure 14.22).24 Although the applications may be more pertinent to patients in the intensive care unit, some have found it useful during liver transplantation surgery in predicting the viability of the organ once in the recipient. It might also be useful in the early detection of a hypermetabolic state in a patient under general anesthesia (e.g. malignant hyperthermia) and distinguishing it from insufflation of CO2 during a laparoscopy procedure.

Carbon dioxide The introduction of CO2 monitoring into clinical practice is one of the major advances in patient safety. Prior to its introduction, many cases of esophageal intubation were unrecognized, leading to adverse outcomes, not to mention increases in malpractice premiums. Detection of CO2 on a breath-by-breath basis is considered to be the best method to confirm endotracheal intubation.25 The applications of CO2 monitoring (capnography) are numerous; entire textbooks have been devoted to this subject.26,27 A normal capnogram is depicted in Figure 14.23. The normal capnogram is divided into four phases. Phase I (A–B) is the inspiratory baseline, which is normally zero. Phase II (B– C) is the expiratory upstroke. This is normally steep. As the 50 III

37

D C

II I

IV A

B

E

0 Figure 14.23. Normal capnogram; see text for details. Capnograms by permission of Jaffe MB and Novametrix Inc., Wallingford, CT. Courtesy of Philips-Respironics.

Decreased removal (hypoventilation) Rebreathing (exhausted absorbent, channeling, incompetent unidirectional valves, CO2 delivered to circuit in fresh gas flow) Hyperventilation, decreased CO2 production/delivery to lungs, low CO, V/Q mismatch, increased alveolar dead space, pulmonary embolism, artifactual (rapid shallow breaths, gas sampling rate⬎expiratory flow rate, miscalibration of analyzer, air leak into sampling system

Source: By permission of Jaffee MB and Novametrix Inc., Wallingford, CT. Courtesy of Philips-Respironics.

patient exhales, fresh gas in the anatomic dead space (with no carbon dioxide) is gradually replaced by carbon dioxidecontaining gas from the alveoli. Phase III (C–D) is the expiratory plateau, which normally has a slight upward gradient. This is because there is not perfect matching of ventilation and perfusion throughout the lungs. Alveoli with lower V/Q ratios – and, therefore, higher carbon dioxide concentrations – tend to empty later during exhalation than those with high V/Q ratios. When exhalation is complete, the plateau continues because exhaled carbon dioxide from the alveoli remains at the gas sampling site until the next inspiration. The end-tidal carbon dioxide concentration (PE CO 2 ) is considered to be the same as the alveolar concentration (PACO2 ). Phase IV (D–E) is the inspiratory downstroke, as fresh gas replaces alveolar gas at the sampling site. The presence of a normal capnogram indicates that the lungs are being ventilated. The ventilation may be spontaneous, assisted, or controlled. The inspired CO2 concentration is normally zero, and the end-tidal normally between 34 and 44 mmHg. Table 14.2 shows some of the possible causes for values outside the normal ranges. Abnormalities by phases of the capnogram are shown in Table 14.3. Observation of the shape of the capnogram may also be helpful in alerting the caregiver to certain conditions. Examples of abnormal capnograms are shown in Figures 14.24 through 14.31. The end-tidal CO2 concentration is commonly used as a surrogate for alveolar CO2 tension, which in turn is used to track arterial CO2 , a value that must be obtained invasively. There is normally an arterial-to-end-tidal CO2 tension difference of about 4 mmHg. This difference is not constant and is affected by the alveolar dead space (DSA), which is the portion of the alveolar ventilation (VA) that is wasted.28 Consider the following example of a patient whose lungs are being ventilated:

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Monitoring in Anesthesia and Perioperative Care

Table 14.3.

Capnogram abnormalities by phase

Abnormality Phase I Increased FICO2

Phase II Slow/slanted

Phase III Irregular

Regular

CO2 (mmHg) 50

Real-time

Possible Causes

37

Rebreathing of CO2 (exhausted absorbent, channeling, incompetent inspiratory/expiratory unidirectional valve(s), CO2 delivered to circuit in fresh gas flow (some machines have CO2 flowmeters), CO2 gas being delivered via N2 O pipeline, inadequate fresh gas flow in Mapleson (rebreathing) circuit, Bain circuit inner tube disconnect, capnograph analyzer not calibrated

Figure 14.27. Abnormal capnogram: expiratory obstruction or bronchospasm. Courtesy of Philips-Respironics.

Exhalation gas flow obstruction (mechanical or in patient), kinked tracheal tube, bronchospasm, gas sampling rate poorly matched to exhalation flow rate, exhaled CO2 becomes more quickly diluted by fresh gas. Mechanical impingement on chest or abdomen by surgeons; patient attemping to breathe sponataeously while lungs are being mechanically ventilated (“curare cleft”) Cardiac oscillations; after exhalation complete, blood pulsating in chest moves gas forward and backward past sampling site. Slow decay of end-tidal gas sampling during expiratory pause causes CO2 to be gradually diluted by fresh gas.

0

CO2 (mmHg) 50

Real-time

37

0

Figure 14.28. Abnormal capnogram: spontaneous efforts of breathing during positive-pressure ventilation (“curare clefts”). Courtesy of PhilipsRespironics. CO2 (mmHg) 50

Real-time

37

0

Phase IV Widened, slurred downstroke, not reaching baseline Incompetent inspiratory valve; CO2 accumulated in inspiratory limb mixed with fresh gas gradually replaced by fresh gas.

Source: By permission of Jaffe MB and Novametrix, Inc., Wallingford, CT. Courtesy of Philips-Respironics.

CO2 (mmHg) 50 37

Figure 14.29. Abnormal capnogram: cardiac oscillations. Courtesy of Philips-Respironics. CO2 (mmHg) 50 37

0

Figure 14.30. Abnormal capnogram: esophageal intubation. Courtesy of Philips-Respironics. A

0

Figure 14.24. Abnormal capnogram: CO2 increasing. Courtesy of PhilipsRespironics. CO2 (mmHg) 50 37

50

0 5

15

10

15

B

0

Figure 14.25. Abnormal capnogram: CO2 decreasing. Courtesy of PhilipsRespironics.

10

50

CO2 (mmHg) 50

37 0 5

0

Figure 14.26. Abnormal capnogram: rebreathing of CO2 Courtesy of Philips-Respironics.

166

Figure 14.31. Abnormal capnogram: circle breathing system with (A) incompetent inspiratory valve; (B) incompetent expiratory valve. Note that there is more rebreathing of CO2 with an incompetent expiratory valve. Courtesy of Philips-Respironics.

Chapter 14 – Respiratory Gas Monitoring

PaCO2 40 mmHg, end-tidal (alveolar, PA) CO2 36 mmHg, tidal volume 500 mL, anatomical dead space 150 mL; therefore, alveolar tidal ventilation (VA) is (500 − 150) = 350 mL. DSA/VA = (PaCO2 − PACO2 )/PaCO2 = (40 − 36)/40 = 10% Thus, 350 × 10% = 35 mL of the alveolar tidal ventilation is alveolar dead space or wasted ventilation. In addition to its use for confirming tracheal rather than esophageal intubation, and to make adjustments to ventilator settings, end-tidal CO2 monitoring has been found to correlate well with cardiac output during low flow states. This has been applied in the evaluation of the efficacy of resuscitation efforts in cardiac arrest victims. Several studies have found that a low end-tidal CO2 is associated with a poorer prognosis.29,30

Nitrogen When available, measurement of nitrogen is useful in following preoxygenation (nitrogen washout) and detecting venous air embolism and air leaks into the anesthesia breathing system. Fortunately, alternative means are now available to perform these functions.

Potent inhaled anesthetic agents and nitrous oxide Contemporary multigas analyzers measure the inspired and end-tidal concentrations of N2 O as well as the potent agents desflurane, enflurane, halothane, isoflurane, and sevoflurane in the presence of one another. Although no study has established the value of this monitoring modality, the possible applications make the potential benefits of its use obvious. Thus it makes possible the monitoring of anesthetic uptake and washout, as well as setting high and (if desired) low alarm limits for agent concentrations. By adding the minimum alveolar concentration (MAC) values for N2 O and the potent agents to the analyzer software, and because MAC values are additive, once the composition of the gas mixture is known, a (total) MAC value can be displayed (Figure 14.21). This may be useful as an indication of anesthetic depth and a form of awareness monitoring. Monitoring agent levels during uptake permits a safer and more intelligent use of the anesthesia vaporizer to reach target end-tidal concentrations in the patient. A high fresh gas flow and vaporizer concentration dial setting will ensure that the gas composition in the circuit changes rapidly; the technique of overpressure can be used to speed anesthetic uptake. When the desired end-tidal concentration has been attained, the vaporizer concentration dial setting can be decreased. When equilibrium has been reached – that is, inspired and end-tidal agent concentrations are almost equal – the fresh gas flow can be decreased to maintain the equilibrium and conserve anesthetic agent. Monitoring of the anesthetic concentration during

elimination provides information as to the state of its washout. The washout rate might then be increased by increasing the fresh gas flow, and hence removal into the waste gas scavenging system. The anesthetic agent high-concentration alarm can be used to alert to potential anesthetic overdosing. The ASA Closed Claims Project includes several adverse outcomes resulting from anesthetic overdose, and there are other reports of vaporizer malfunction leading to higher-than-intended output concentrations.31,32 The low-concentration alarm can be used to help prevent awareness by maintaining an anesthetic agent concentration that exceeds MACawake. The latter is the average of the concentrations immediately above and below those permitting voluntary response to command.33 MACawake is approximately one-third of MAC.34 The anesthetic agent low-concentration alarm will also serve as a late sign that the vaporizer is becoming empty. An agent analyzer may also alert to an air leak into the breathing system that is causing an unintended low agent concentration.35 Assuming that the analyzer has been calibrated according to the manufacturer’s instructions, it can be used to check the calibration of a vaporizer, as well as detect mixed agents in a vaporizer. Monitoring of N2 O concentrations may be helpful when one is discontinuing or avoiding its administration. This may apply in patients who have closed air spaces that might expand with the use of N2 O. The continuous analysis of all of the respired gases by a multigas monitor also facilitates recording of the data by an automated anesthesia information management system. Many anesthesia caregivers find it useful to record end-tidal concentrations of the gases administered. Monitoring of agent concentration, fresh gas flow, and time facilitates calculation of the consumption of the potent agents, both in liters of vapor or in milliliters of liquid agent. Attention to these data might be used to promote the more economical use of the more expensive anesthetics.

Complications The complications associated with respiratory gas monitoring can be divided into two categories: pure equipment failure and use(r) error.31 As with any mechanical or electronic piece of equipment, failure can occur but, overall, the devices are very reliable if properly maintained. This includes any recommended maintenance and calibration procedures. Use(r) error is a much more common problem. The user must understand respiratory physiology, as well as the monitoring technology; otherwise, he or she may not recognize a spurious reading or may misinterpret data. This can lead to an inappropriate change in patient management. A simple example is that a low end-tidal CO2 reading may cause the user to assume that the cause is hyperventilation and to decrease ventilation, when the problem is really a low cardiac output state.

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In the event of total failure of the capnograph (electrical, mechanical, optical, and so forth) one should always keep a colorimetric CO2 detector as an immediate backup. Because these devices have an expiration date shown on the packaging, they should be checked routinely and replaced as necessary. For greater accuracy, an arterial blood sample can be drawn for analysis in a blood gas analyzer.

Credentialing At the time of writing, there is no specific credentialing requirement associated with the use of gas monitoring. All users should receive in-service training when a new monitor is introduced, and, in particular, they should understand and use the alarm features. Unfortunately, this is often not the case. There is no doubt that an educated user will derive more benefit than one who has less understanding of the equipment. In this regard, the Anesthesia Patient Safety Foundation (APSF) has sponsored a technology training initiative to promote critical training on new, sophisticated, or unfamiliar devices that can directly affect patient safety. 36

Practice parameters In 1986, the ASA first approved its Standards for Basic Anesthesia Monitoring. These have undergone periodic review and modification, the most recent being on October 20, 2010 with an effective date of July 1, 2011.37 The following bolded sections are quoted directly from Standard II of the ASA Standards for Basic Anesthetic Monitoring, and pertain to the contents of this chapter. STANDARD II During all anesthetics, the patient’s oxygenation, ventilation, circulation and temperature shall be continually evaluated.

York38 and New Jersey. The standard does not demand use of any specific technology to make the measurement, nor does it specify where in the inspiratory path oxygen must be monitored. Thus it is common to have a fuel cell located in the inspiratory unidirectional valve housing, but downstream (on the patient side) of the valve. It is also acceptable to sample gas from a connector by the patient’s airway at the Y-piece for oxygen analysis in a multigas analyzer. VENTILATION OBJECTIVE To ensure adequate ventilation of the patient during all anesthetics. METHODS l) Every patient receiving general anesthesia shall have the adequacy of ventilation continually evaluated. Qualitative clinical signs such as chest excursion, observation of the reservoir breathing bag and auscultation of breath sounds are useful. Continual monitoring for the presence of expired carbon dioxide shall be performed unless invalidated by the nature of the patient, procedure or equipment. Quantitative monitoring of the volume of expired gas is strongly encouraged.∗ When an endotracheal tube or laryngeal mask is inserted, its correct positioning must be verified by clinical assessment and by identification of carbon dioxide in the expired gas. Continual end-tidal carbon dioxide analysis, in use from the time of endotracheal tube/laryngeal mask placement, until extubation/removal or initiating transfer to a postoperative care location, shall be performed using a quantitative method such as capnography, capnometry or mass spectroscopy.∗ When capnography or capnometry is utilized, the end tidal CO2 alarm shall be audible to the anesthesiologist or the anesthesia care team personnel.∗ 3) When ventilation is controlled by a mechanical ventilator, there shall be in continuous use a device that is capable of detecting disconnection of components of the breathing system. The device must give an audible signal

OXYGENATION

when its alarm threshold is exceeded.

OBJECTIVE To ensure adequate oxygen concentration in the inspired gas and the blood during all anesthetics. METHODS l) Inspired gas: During every administration of general anesthesia using an anesthesia machine, the concentration of oxygen in the patient breathing system shall be measured by an oxygen analyzer with a low oxygen concentration limit alarm in use.∗ [† Note that “continual” is defined as “repeated regularly and frequently in steady rapid succession” whereas “continuous” means “prolonged without any interruption at any time.”] • Under extenuating circumstances, the responsible anesthesiologist may waive the requirements marked with an asterisk (∗ ); it is recommended that when this is done, it should be so stated (including the reasons) in a note in the patient’s medical record.]

The requirement to monitor the FIO2 in the breathing system is not only one of the ASA standards, but it is also included in the health code regulations of some states, including New

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4) During regional anesthesia (with no sedation) or local anesthesia (with no sedation), the adequacy of ventilation shall be evaluated by continual observation of qualitative clinical signs. During moderate or deep sedation the adequacy of ventilation shall be evaluated by continual observation of qualitative clinical signs and monitoring for the presence of exhaled carbon dioxide unless precluded or invalidated by the nature of the patient, procedure, or equipment.

The ASA standards applicable to CO2 monitoring have evolved considerably since they were first written. In particular, they have been revised to include use of the laryngeal mask airway (a supraglottic airway device), as well as use in regional anesthesia and monitored anesthesia care. Note that in item 3, the capnograph could be considered a disconnect detection device and as such must be used with an audible alarm activated. Catastrophes have been reported when state-of-the-art monitoring has been used, but with the alarms silenced.39 At the time of this writing, there is no ASA standard that requires monitoring of N2 O and the potent inhaled anesthetics. However, as use of this monitoring becomes more widespread,

Chapter 14 – Respiratory Gas Monitoring

it may become a de facto standard.40 The manufacturers of anesthesia workstations anticipate this trend; the most recent American Society for Testing and Materials (ASTM) voluntary consensus standard requires that the anesthesia workstation be provided with a device to monitor the concentration of anesthetic vapor in the inspired gas.41 The ASA standards for postanesthesia care (last updated in 2004)42 do not require monitoring of gas concentrations. ASA STANDARDS FOR POSTANESTHESIA CARE STANDARD IV THE PATIENT’S CONDITION SHALL BE EVALUATED CONTINUALLY IN THE PACU. 1. The patient shall be observed and monitored by methods appropriate to the patient’s medical condition. Particular attention should be given to monitoring oxygenation, ventilation, circulation, level of consciousness and temperature. During recovery from all anesthetics, a quantitative method of assessing oxygenation such as pulse oximetry shall be employed in the initial phase of recovery.∗ This is not intended for application during the recovery of the obstetrical patient in whom regional anesthesia was used for labor and vaginal delivery.

In many postanesthesia care units (PACUs), however, capnometry is used in patients who are tracheally intubated. If a patient requires reintubation, means to confirm tracheal placement of the tube should be available and its use documented.

Acknowledgment The author is grateful to Dr. Daniel Raemer and Dr. Michael Jaffe for reviewing this chapter and for their valuable contributions.

References 1. Mushlin PS, Mark JB, Elliott WR et al. Inadvertent development of subatmospheric airway pressure during cardiopulmonary bypass. Anesthesiology 1989;71:459–62. 2. Pattinson K, Myers S, Gardner-Thorpe C. Problems with capnography at high altitude. Anaesthesia 2004;59:69–72. 3. Ozanne GM, Young WG, Mazzei WJ, et al. Multipatient anesthetic mass spectrometry. Anesthesiology 1981;55:62-7. 4. Eisenkraft JB, Raemer DB. Monitoring gases in the anesthesia delivery system. In Ehrenwerth J, Eisenkraft JB, eds. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby-Year Book, 1993, p. 210. 5. Steinbrook RA, Elliott WR, Goldman DB, Philip JH. Linking mass spectrometers to provide continuing monitoring during system failure. J Clin Monit 1991;7:271–3. 6. Severinghaus JW, Larson CP, Eger EI. Correction factors for infrared carbon dioxide pressure broadening by nitrogen, nitrous oxide, and cyclopropane. Anesthesiology 1961;22:429–32. 7. Nielsen JR, Thornton V, Dale EB. The absorption laws for gases in the infrared. Rev Mod Physics 1944;16:307–24. 8. Raemer DB, Philip JH. Monitoring anesthetic and respiratory gases. In Blitt CD, ed. Monitoring in Anesthesia and Critical Care Medicine, New York: Churchill-Livingstone, 1990, pp. 373–86. 9. PB 254 Owners Manual. Puritan-Bennett Corp., Wilmington, MA, 1985.

10. Datex-Ohmeda Compact Airway Modules Technical Reference Manual. Document 800 1009–5. Datex-Ohmeda Division, Instrumentarium Corp., Finland, 2003 (accessed February 20, 2011). 11. Møllgaard K. Acoustic gas measurement. Biomed Instr Technol 1989;23:495–7. 12. Westenskow DR, Smith KW, Coleman DL, et al. Clinical evaluation of a Raman scattering multiple gas analyzer for the operating room. Anesthesiology 1989;70:350–5. 13. Colman Y, Krauss B. Microstream capnography technology: a new approach to an old problem. J Clin Monit Comput 1999;15:403–9. 14. Casati A, Gallioli A, Passarretta P, Borgi B, Torri G. Accuracy of end-tidal carbon dioxide monitoring using the NPB 75 Microstream capnometer. A study in intubated, ventilated and spontaneously breathing nonintubated patients. Eur J Anaesthesiol 2000;17:622–6. 15. Severinghaus JW. Water vapor calibration errors in some capnometers: respiratory conventions misunderstood by manufacturers? Anesthesiology 1989;70:996–8. 16. Sum Ping ST, Mehta MP, Symreng T. Accuracy of the FEF CO2 detector in the assessment of endotracheal tube placement. Anesth Analg 1992;74:415–9. 17. Srinivasa V, Kodali BS. Caution when using colorimetry to confirm endotracheal intubation. Anesth Analg 2007;104: 738. 18. Brackney SM, Bennett NP. Caution when using colorimetry to confirm endotracheal intubation. Anesth Analg 2007;104:739. 19. Fontijn A, Sabadell AJ. Ronco RJ. Homogeneous chemiluminescent measurement of nitric oxide with ozone. Analyt Chem 1979;42:575–9. 20. Holland R. Wrong gas disaster in Hong Kong. APSF Newsletter 1989;4:25–36. 21. Berry CB, Myles PS. Preoxygenation in healthy volunteers: a graph of oxygen “washin” using end-tidal oxygraphy. Br J Anaesth 1994;74:116–8. 22. Barnard JP, Sleigh JW. Breath-by-breath analysis of oxygen uptake using the Datex Ultima. Br J Anaesth 1995;74: 155–8. 23. Takala J. Meril¨ainen P. Handbook of Indirect Calorimetry and Gas Exchange. Helsinki, Finland: Datex-Ohmeda, 876710–01, 2001, p. 30. 24. Takala J. Appliguide. Clinical application guide of gas exchange and indirect calorimetry. Helsinki, Finland: Datex-Ohmeda 895143–1, 2000. 25. Birmingham PK, Cheney FW, Ward RJ. Esophageal intubation: a review of detection techniques. Anesth Analg 1986;65:886–91. 26. Gravenstein JS, Jaffe MB, Paulus DA. Capnography: Clinical Aspects. New York: Cambridge University Press, 2004. 27. Smalhout B, Kalenda Z. An Atlas of Capnography. 2nd ed. Utrecht, The Netherlands: Kerkebosche Zeist, 1981. 28. Nunn JF. Applied Respiratory Physiology. Boston: Butterworths, 1977, p. 226. 29. Sanders AB, Kern KB, Otto CW Milander MM, Ewy GA. End-tidal CO2 monitoring during CPR. A prognostic indicator for survival. JAMA 1989;262:1347–51. 30. Wayne ME, Levine RL, Miller CC. Use of end-tidal CO2 to predict outcome in pre-hospital cardiac arrest. Ann Emerg Med 1995;25:762–7. 31. Caplan RA, Vistica MF, Posner KL, Cheney FW. Adverse anesthetic outcomes arising from gas delivery equipment: a closed claims analysis. Anesthesiology 1997;87:741–8.

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32. Geffroy JC, Gentili ME, Le Poll`es R, Triclot P. Massive inhalation of desflurane due to vaporizer dysfunction. Anesthesiology 2005;103:1096–8. 33. Stoelting RK, Longnecker DE, Eger EI II. Minimal alveolar concentrations on awakening from methoxyflurane, halothane, ether and fluroxene in man: MAC awake. Anesthesiology 1970;33:5–9. 34. Eger EI II, Weisskopf RB, Eisenkraft JB. The Pharmacology of Inhaled Anesthetics. San Antonio, TX: Dannemiller Memorial Educational Foundation, 2002, p. 27. 35. Sandberg WS, Kaiser S. Novel breathing system architecture: new consequences of old problems. Anesthesiology 2004;100: 755–6. 36. Olympio MA. Formal training and assessment before using advanced medical devices in the OR. APSF Newsletter 2007;22:63–65.

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37. American Society of Anesthesiologists. Standards for Basic Anesthetic Monitoring. http://www.asahq.org/publications AndServices/standards/02.pdf (accessed February 20, 2011). 38. NY State Laws and regulations,section 405.13. Anesthesia services (b)(2)(iii)(d). 39. $16 million settlement. Monitoring devices turned off/down: patient suffers irreversible brain damage. Anesthesia Malpractice Prevention Newsletter 1997;2(3)1. 40. Eichhorn JH. Pulse oximetry as a standard of practice in anesthesia. Anesthesiology 1993;78:423–5. 41. Standard Specification for Particular Requirements for Anesthesia Workstations and their Components ASTM F1850–2005. West Conshohocken, PA: American Society for Testing and Materials, 2005. 42. ASA Standards for postanesthesia care. http://www.asahq.org/ publicationsAndServices/standards/36.pdf.

Chapter

15

Monitoring pressure, volume, and flow in the anesthesia breathing system James B. Eisenkraft

Introduction The anesthesia breathing system is an enclosed environment with which the patient makes respiratory gas exchange. By controlling the composition of the gases in the breathing circuit, as well as ventilatory parameters, the anesthesia caregiver can control the tensions of oxygen, carbon dioxide, nitrogen, and the inhaled anesthetics in the patient’s arterial blood. Monitoring of the respired gases has been discussed in Chapter 14. This chapter addresses the monitoring of pressures, volumes, and gas flows in the breathing system. Monitoring of these parameters is important in enhancing the safety of ventilation and verifying the appropriateness of ventilatory settings.

Measurement of respiratory pressures, volumes, and flows Pressure Pressure is defined as force per unit area (e.g. pounds per square inch), although the units of the denominator are often omitted, as they are assumed to be understood (as in mmHg or cmH2 O). Pressures are usually measured using either a simple mechanical device or an electromechanical transducer. Simple analog gauges have been commonly used to measure and display breathing system pressure. These gauges are termed aneroid (meaning without fluid) gauges. The gauge may be based on a Bourdon tube (Figure 15.1), diaphragm, or bellows (Figure 15.2). In the Bourdon tube design, an indicator needle mechanism is attached to the closed, free end of a curved piece of flattened soft metal tubing. The open end of the tubing is in communication with the breathing circuit. Pressure in the circuit causes the flattened tubing to become more circular. This causes the tubing to uncoil and move the indicator needle mechanism (Figure 15.1). A small adjustment screw is often used to align the indicator needle to the zero-pressure mark when the gauge is exposed to atmosphere. A high-quality Bourdon tube is accurate and reliable, and requires no mechanical stop at zero. Excessive pressures can bend the malleable tubing or indicator needle mechanism, thus rendering the device inoperable, but such pressures are unlikely to be encountered in a breathing system. The gauge is usually calibrated to measure negative as well as positive pressures.

The principle of the bellows pressure gauge is that the volume of a bellows changes according to the pressure that is applied to it. If the bellows is sealed, its volume is a function of the ambient or surrounding pressure (Figure 15.2A). If the interior of the bellows is in communication with the breathing system, the volume of the bellows is determined by the difference in pressures across the bellows (Figure 15.2B), and is termed gauge pressure. The advantage of the analog pressure gauge is that it is simple and mechanical, and requires no warmup time or electrical energy to function. Such gauges were widely used on traditional anesthesia machines. Disadvantages are that they cannot be interfaced with electronic anesthesia care stations or to trigger alarms. Although modern electronic anesthesia care stations use sophisticated electronic pressure transducers to measure pressures, some manufacturers still offer a mechanical analog gauge as an optional extra. Contemporary anesthesia workstations use electromechanical transducers to measure pressure. When used in combination with pneumotachometers, Pitot tubes, or variable orifices, the pressure measurements can be used to measure gas flows and volumes. The most common electromechanical transducer is the metal or semiconductor strain gauge. When a metal wire or thin segment of semiconductor material is stretched within its elastic limit, its resistance is altered because of dimensional changes and a change in the material’s resistivity. The change in

100 50

150

0

200

Figure 15.1. Bourdon tube pressure gauge. From Davis PD, Parbrook GD, Kenny GNC. Basic Physics and Measurement in Anesthesia, 4th ed. Boston: Butterworth Heinemann, 1995, with permission.

Pressure

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Absolute pressure

Gauge or differential pressure

Pressure

Sapphire posts Stationary structural member

PB

PB

Pressure to be measured A

B

Figure 15.2. Bellows-based pressure gauges. A: The bellows is sealed and therefore measures absolute or atmospheric pressure (PB ). B: The bellows is connected to the system whose pressure is to be measured and therefore measures pressure in relation to ambient (PB ). From Davis PD, Parbrook GD, Kenny GNC. Basic Physics and Measurement in Anesthesia, 4th ed. Boston: Butterworth Heinemann, 1995, with permission.

resistivity is called the piezoresistive effect. Fine wires made from such alloys as constantan, nichrome, and karma are particularly appropriate for metal strain gauges. In one common design, the bonded-wire strain gauge, the wires are cemented to a backing (Figure 15.3). A flexible diaphragm attached to the bonded-wire strain gauge is exposed to the pressure to be measured on one side and the ambient pressure on the other. As the diaphragm bends, the wires are stretched and the change in resistance corresponding to the change in pressure is measured.

Connection leads Backing P

Stretch

P

Pam

Strain gauge wire bonded to backing

Flexible diaphragm Pam

Figure 15.3. Bonded wire strain gauge. A length of metal strain gauge wire is cemented to a backing that is fixed at one end. As pressure is applied to the flexible diaphragm, the backing and strain gauge wire are stretched. The change in resistance of the wire is measured and displayed as a change in pressure. P, applied pressure; Pam , ambient pressure. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993.

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Strain gauge wire element

Moving structural member

Figure 15.4. Top view of an unbonded-wire strain gauge. Lengths of strain gauge wire are stretched between posts on two supporting structural members. The outer structural member is stationary. When pressure is applied in the direction of the arrow, the center structural member moves incrementally. One pair of strain gauge wires is stretched further, and the other is relaxed. The resulting change in resistance of the four elements is measured using a Wheatstone bridge circuit and displayed as pressure. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

In another design (Figure 15.4), two pairs of wires are attached to posts of two structural members that can move with respect to each other. One of the structural members is mechanically attached to a pressure-sensing diaphragm. When the diaphragm moves as a response to applied pressure, two of the wires are stretched and the other pair is relaxed. The changes in the resistances of the four wires are then measured using a Wheatstone bridge circuit. In the semiconductor strain gauge, the materials used are usually crystals of silicon or germanium. A flexible diaphragm is etched into the crystal by integrated circuit techniques. A system of four silicon elements is produced in the diaphragm in such a way that the elements change predictably in resistance value as the diaphragm is deformed. During manufacture, the resistance elements are trimmed dimensionally with a laser, and so no further calibration is required. The advantage of semiconductor materials is that they exhibit 50 to 100 times the change in resistance per unit of strain compared to metals.1 However, the temperature sensitivity is substantially greater in semiconductor gauges, and accurate compensation is a major factor in their design. In both the metal and semiconductor strain gauges, the change in resistance of the elements is measured via an electrical circuit called a Wheatstone bridge (Figure 15.5). This arrangement is particularly useful for several reasons. First, the Wheatstone bridge allows the simultaneous measurement of resistance

Chapter 15 – Monitoring Pressure, Volume, and Flow in the Anesthesia Breathing System

A

Tangential slits to direct gas flow toward rotating vane R2

R1 + D

C VOLTS R3

Gas inflow

R4

B Figure 15.5. Wheatstone bridge circuit used for strain gauge transducers. Voltage from a battery is applied between points A and B. One or more of the variable resistors shown (R1–R4) are resistance elements of the transducer. The remaining resistor values are selected so that the voltage difference measured between points C and D is very small, or “balanced,” when zero pressure is applied to the transducer. As the pressure applied to the transducer changes, the bridge becomes “unbalanced,” and a voltage appears between points C and D. Appropriate selection of resistance elements and temperature-sensitive elements as resistors in the Wheatstone bridge can result in highly sensitive, temperature-compensated measurement. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

changes in multiple elements when they are used as legs of the bridge. Second, temperature compensation can be incorporated directly into the bridge by way of metal or semiconductor elements that are sensitive to temperature but not exposed to the strain. Third, a small change in resistance can be measured as a relative change in voltage near zero between the two balance points of the bridge.

Volume and flow Flow is defined as volume per unit of time; therefore, measurement of flow and time permits calculation of volume. Like pressure, flow can be measured using a simple mechanical device or by electronic means.

Mechanical The simplest flow measurement device is the vane anemometer. This was originally introduced into respiratory measurement by B. Martin Wright in England.2 Using adaptors, this is a freestanding device that can be inserted into the breathing system, where it is commonly used to measure tidal volume and minute ventilation. This device uses a low-mass rotating vane in the gas stream (Figure 15.6). Gas molecules colliding with the blades of the vane transfer their momentum in the direction of flow and cause the vane to rotate. In the mechanical version, the rotation of the vane is connected to the dial via a gear mechanism, similar to that in a watch. In an electronic implementation (Figure 15.7), two pairs of light-emitting diodes (LEDs) and silicon photodetectors are used to measure the rate and direction of the vane’s rotation. The rotation rate is integrated electronically to determine the volume of gas passing the transducer over time.

Rotating vane Figure 15.6. Wright’s respirometer. Respired gas is directed through oblique slots in a small cylinder enclosing a small vane that is made to rotate. The spindle on which the vane is mounted drives a gear train connected to a pointer that moves over a dial indicating the volume of gas passed. Gases that flow back through the device do not register because they enter along the axis of the vane spindle.

A number of physical factors limit the accuracy of the vane anemometer.3 Because the principle of operation is momentum, the density of the gas affects the measurement. The gas flow is directed to the blades of the vane by tangential slots; thus, the viscosity of the gas also influences the measurement. Additionally, inertia and momentum of the vane are problematic. Accuracy is poor at low flows because of inertia, and at high flows because of momentum. Pulsatile flows also cause overreading. The accuracy of the Wright respirometer has been shown to be within ± 10 percent during anesthesia. The respirometer is compact and is easily placed between the breathing system and the patient. However, the mechanical version cannot measure bidirectional flow and, because it is mechanical, it has no alarms. A sealed mechanical volumeter (Figure 15.8) was used by Dr¨ager in some older delivery systems to measure tidal volume and minute ventilation. This device consists of a pair of rotating elements in the gas flow path, configured much like a revolving door at the entrance to a building. A fixed volume of gas is passed across the volumeter with each quarter-rotation of the dumbbell-shaped elements. A seal is formed between the polystyrene rotating elements and the interior wall of the tube. The sealed volumeter provides substantially more resistance to flow than does the vane anemometer. The accuracy of the volumeter is affected by gas density and by the inertia of the rotating elements. However, it is not influenced substantially by the flow pattern of the gas. The number of fixed volumes of gas transferred from inlet to outlet is measured mechanically. The Dr¨ager Spiromed is an electronic version of the mechanical spirometer. Gas flow through the device determines the rate of rotation of the rotors, which is measured

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Figure 15.7. Vane anemometer. Gas flow is directed by fixed vanes at the inlet, and the swirling gas causes rotation of a low-mass vane. LEDs are positioned to detect the revolutions of the vane, which are converted into a measurement of flow. This type of anemometer is used in the spirometer on the Ohmeda Modulus anesthesia machines. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

Outflow gas

Shaft

Inflow gas

Fixed blades

Low-mass vane

Fixed blades

using an electromagnetic sensing system. The Spiromed is direction-sensitive, and can alert to reversal of gas flow in the circle system. The accuracy of the Spiromed for tidal volumes is ± 40 mL, and for minute ventilation, ± 100 mL or ± 10 percent of the reading.

Rolling seals

Inflow gas

Outflow gas

Figure 15.8. Sealed volumeter. Polystyrene rotating elements form a seal against the interior of the volumeter. Gas flow causes rotation of the elements, transferring fixed volumes of gas from the inlet to the outlet. Measured volume is displayed on a gauge that is mechanically connected to the rotating shaft of the volumeter. The device is bidirectional, and can alert to reversed flow. If the number of fixed volumes of gas transferred is measured electronically, measured volume may be read on a remote display, as well as being connected to an alarm system. This is the principle of operation of the Dr¨ager Spiromed. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

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Pneumotachometer The principle of operation of the pneumotachometer is to measure the loss of energy of the flowing gas as it passes through a resistive element. The resistive element is designed to ensure that the flow of gas is laminar so the energy loss is completely the result of viscosity and the flow is directly proportional to the pressure difference. The energy loss is measured as a pressure difference from the inlet to the outlet of the resistive element. The most common type of resistive element, designed by Fleish,4 consists of narrow, parallel metal tubes aligned in the direction of the flow (Figure 15.9). Nominally, for laminar flow, the pneumotachometer obeys the Hagen-Poiseuille law: F = [␲ × r 4 × (P1 − P2]/[8 × ␩ × L], where F = gas flow, r and L = radius and length of the element, P1 and P2 = inlet and outlet pressures, and ␩ = viscosity of gas flowing through the device. Measurement of flow is independent of gas density and total pressure. Fleish pneumotachometers have been used widely in respiratory physiology and pulmonary function studies, and are available in various sizes (resistances) to accommodate the appropriate flow range. The resistance of the element must be chosen so the pressure difference produced in the flow range of interest is large enough to be measured accurately by the available pressure transducer(s). Too resistive an element will impede ventilation. The Fleish pneumotachometer usually uses a heating element to raise the temperature of the device to about 40◦ C, thus preventing condensation of moisture in expired gas.

Chapter 15 – Monitoring Pressure, Volume, and Flow in the Anesthesia Breathing System

P1

Heater

P2

Laminar flow elements

A

respiratory gases in the range of 20◦ C to 40◦ C, although the linear coefficient is different for each gas. The other disadvantage of the pneumotachometer in an anesthesia circuit is its propensity to accumulate mucus and water in its narrow tubes. It must be repeatedly calibrated because its effective resistance changes with fouling. In addition, the pneumotachometer must be cleaned and sterilized between clinical uses.

Pitot tube flowmeter

B Figure 15.9. Cross-sectional views of a Fleisch pneumotachometer. (A) Longitudinal section showing the parallel paths that constitute the laminar flow resistance element. Ports P1 and P2 are used for measurement of the pressure differential across the resistance element. The device can be used bidirectionally. The heating element surrounds the device and is used to prevent condensation. (B) Cross-sectional view of laminar flow elements. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

The pressure difference across the resistive element (or head) is measured using a differential pressure transducer with sufficient sensitivity and frequency response. The transducer must be zeroed (nulled) electronically by reserving a measurement made with zero flow. The pressure difference is typically in the range of 2 cmH2 O. Pressure transducer output readings tend to drift, and the measured signal is small; therefore, they must be renulled periodically. For vigorous ventilatory flows, the rate of change in gas flow is great, and the frequency response of the transducer must be adequate to follow these changes. The respiratory volume is computed by integrating the flow with respect to time (because flow = volume/time). The pneumotachometer is calibrated by setting a gain coefficient according to a volume produced by manually emptying a calibrated (usually 1 L) syringe through the device. Often, the calibration syringe is emptied several times at different rates to simulate the range of gas flows expected during clinical use. In practice, the characteristics of the Fleish pneumotachometer are dependent on the geometry of the tubing on the upstream side of the resistive element. This results in a distinctly nonlinear deviation from the Hagen-Poiseuille law. The viscosity of gases in the respiratory mixture must be taken into consideration if measurement of flow is to be accurate. Consider that the viscosity of a gas mixture of 88.81 percent oxygen, 1.61 percent nitrogen, and 9.58 percent carbon dioxide is 9.1 percent greater than that of air. Thus, substantial errors can result if gas viscosity is not taken into consideration. Temperature is considered to have a linear effect on the viscosity of

The Pitot tube measures the difference in kinetic energy of the gas impinging on a pressure port facing in the direction of the gas flow and on a pressure port perpendicular to the flow.5 The pressure difference, nominally proportional to the square of the flow rate, is sensitive to the density of the gas. Viscous losses around the pressure ports and small pressure differences at low flows are limitations of the Pitot tube flowmeter (Figure 15.10). The GE-Datex Sidestream Spirometry system, as used in the GE S/5 Physiologic Monitoring Systems, represents a combination of Pitot tube and pneumotachograph technologies, with gas analysis technology that provides the gas density and viscosity data required for accuracy. This system uses a patented DLite adapter (Figure 15.11) that is placed in the breathing system between the Y-piece and the patient’s airway. The D-Lite adapter has two Pitot tubes, one facing upstream in the direction of gas flow to measure total pressure (Pt), the other facing downstream in the opposite direction to measure static pressure (Ps; Figure 15.12). The difference (Pt – Ps) is the dynamic pressure, which is proportional to the square of the gas flow rate (see equations that follow). (Pt − Ps) ∝ (flow2 × density)/4, flow2 × density ∝ 4 × (Pt − Ps), flow ∝ 2 × [(Pt – Ps)/density]0.5 . P1

P2

Figure 15.10. Longitudinal cross-section of a Pitot tube flowmeter. The pressure P2 measured at port P2 facing the flow direction is greater than P1 because of the kinetic energy of the gas impinging on the port. The pressure difference (P2-P1) is proportional to the square of the flow rate. From Raemer DB. Monitoring ventilation. In Ehrenwerth J, Eisenkraft JB. Anesthesia Equipment: Principles and Applications. St. Louis: Mosby Year Book, 1993, with permission.

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Monitoring in Anesthesia and Perioperative Care

To differential pressure transducer A

Double-lumen tubing

B

From patient circuit

To patient

Figure 15.11. D-Lite sidestream spirometry adapter (GE Datex-Ohmeda), placed between the Y-piece of breathing system and the connector to the patient’s airway device (tracheal tube, LMA, etc.). The double-lumen tubing connects the Pitot tubes to the differential pressure-sensing elements in the monitoring module.

C

To gas analyzer

Gas sampling tube

During inspiration, as gas flows toward the patient’s airway, the pressure difference between the two Pitot tubes is measured continuously. During exhalation, gas flow through the adapter is reversed and the pressure difference similarly measured. The D-Lite adapter’s two Pitot tubes are connected to the pressure transducers in the monitoring module via a length of noncompliant double-lumen tubing (Figure 15.11). The D-Lite has a third port, to which a gas sampling line that leads to the respiratory gas analyzer in the monitoring module is connected. The continuous analysis of gas composition supplies the density data required for the flow calculation shown earlier.

Signal processing

Gas analysis #2

#1

Pressure sensor

Monitor Display

Hot wire anemometer

3m Tubes Exp.

Insp.

Sensor

Figure 15.12. Schematic of gas flow sensing arrangement used in the DLite airway adapter shown in Figure 15.11. Data from the differential pressure transducers and from the gas analyzer are used to compute flow and volume.

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The Pitot tube flowmeter actually measures gas flow velocity, which can be converted to a volume flow rate if the crosssectional area of the adapter is known. D-Lite adapters are available in two sizes: the adult (dead space volume 9.5 mL) measures tidal volumes of 150 to 2000 mL; the pediatric (Pedi-Lite, dead space 2.5 mL) measures tidal volumes of 15 to 300 mL. Because the two sizes have different cross-sectional areas, the user must ensure that the compact airway gas monitoring module is set appropriately. Erroneous spirometry data result if the sensor size does not correspond with the appropriate software setting. Advantages of the sidestream spirometry system are that it provides continuous data of many respiratory parameters (tidal volume, minute ventilation, airway pressures, compliance, and flow-volume and pressure-volume loops) measured at the patient’s airway. The readings are therefore not affected by changes in compliance in the breathing system. The adapters are robust and disposable. Disadvantages